Publications by authors named "Yuling Qiu"

53 Publications

Arbuscular Mycorrhization Enhances Nitrogen, Phosphorus and Potassium Accumulation in by Modulating Soil Nutrient Balance under Elevated CO.

J Fungi (Basel) 2021 May 5;7(5). Epub 2021 May 5.

Centre of Excellence for Soil Biology, College of Resources and Environment, and Key Laboratory of Eco-Environments in Three Gorges Reservoir Region (Ministry of Education), School of Life Sciences, Southwest University, Chongqing 400716, China.

Effects of arbuscular mycorrhizal fungi (AMF), elevated carbon dioxide (eCO), and their interaction on nutrient accumulation of leguminous plants and soil fertility is unknown. Plant growth, concentrations of tissue nitrogen (N), phosphorus (P), and potassium (K) in 12-week-old nodulated faba bean (, inoculated with bv. NM353), and nutrient use efficiency were thus assessed under ambient CO (410/460 ppm, daytime, 07:00 a.m.-19:00 p.m./nighttime, 19:00 p.m.-07:00 a.m.) and eCO (550/610 ppm) for 12 weeks with or without AM fungus of inoculation. eCO favored AMF root colonization and nodule biomass production. eCO significantly decreased shoot N, P and K concentrations, but generally increased tissue N, P and K accumulation and their use efficiency with an increased biomass production. Meanwhile, eCO enhanced C allocation into soil but showed no effects on soil available N, P, and K, while AM symbiosis increased accumulation of C, N, P, and K in both plant and soil though increased soil nutrient uptake under eCO. Moreover, plant acquisition of soil NO-N and NH-N respond differently to AMF and eCO treatments. As a result, the interaction between AM symbiosis and eCO did improve plant C accumulation and soil N, P, and K uptake, and an alternative fertilization for legume plantation should be therefore taken under upcoming atmosphere CO rising. Future eCO studies should employ multiple AMF species, with other beneficial fungal or bacterial species, to test their interactive effects on plant performance and soil nutrient availability in the field, under other global change events including warming and drought.
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http://dx.doi.org/10.3390/jof7050361DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8148158PMC
May 2021

Human/eukaryotic ribosomal protein L14 (RPL14/eL14) overexpression represses proliferation, migration, invasion and EMT process in nasopharyngeal carcinoma.

Bioengineered 2021 Dec;12(1):2175-2186

Department of Clinical Laboratory, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China.

Although human/eukaryotic ribosomal protein L14 (RPL14/eL14) is known to be associated with a variety of cancers, its role in nasopharyngeal carcinoma (NPC) remains unclear. The aim of this study was to explore the impact of RPL14(eL14) in NPC. The results of quantitative real-time polymerase chain reaction (qRT-PCR), western blot, and immunohistochemical staining revealed that the expression of RPL14(eL14) significantly reduced in NPC tissues and cells. Furthermore, the protein expression of RPL14(eL14) was linked to NPC-related clinical pathological features, including the T and N classification of Tumor Node Metastasis (TNM) staging (all p < 0.05). Cell counting kit-8 (CCK-8) assay and colony formation assay revealed that RPL14(eL14) overexpression repressed NPC cell proliferation. In cell cycle assay, RPL14(eL14) overexpression significantly blocked NPC cells in S phase. Overexpression of RPL14(eL14) repressed cell migration and invasion in NPC as shown by transwell assay and cell scratch healing assay. In addition, RPL14(eL14) was closely correlated with the expression of epithelial-mesenchymal transition (EMT) biomarkers, including E-cadherin, N-cadherin, and vimentin as detected by western blot. In conclusion, our results revealed that RPL14(eL14) may be considered as an antioncogene in NPC, which greatly suppresses cancer progression.
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http://dx.doi.org/10.1080/21655979.2021.1932225DOI Listing
December 2021

Lansoprazole Alone or in Combination With Gefitinib Shows Antitumor Activity Against Non-small Cell Lung Cancer A549 Cells and .

Front Cell Dev Biol 2021 20;9:655559. Epub 2021 Apr 20.

Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin, China.

Lansoprazole (Lpz) is an FDA-approved proton pump inhibitor (PPI) drug for the therapy of acid-related diseases. Aiming to explore the new application of old drugs, we recently investigated the antitumor effect of Lpz. We demonstrated that the PPI Lpz played a tumor suppressive role in non-small cell lung cancer (NSCLC) A549 cells. Mechanistically, Lpz induced apoptosis and G0/G1 cell cycle arrest by inhibiting the activation of signal transducer and activator of transcription (Stat) 3 and the phosphoinositide 3-kinase (PI3K)/Akt and Raf/ERK pathways. In addition, Lpz inhibited autophagy by blocking the fusion of autophagosomes with lysosomes. Furthermore, Lpz in combination with gefitinib (Gef) showed a synergistic antitumor effect on A549 cells, with enhanced G0/G1 cell cycle arrest and apoptosis. The combination inhibited Stat3 phosphorylation, PI3K/Akt and Raf/ERK signaling, affecting cell cycle-related proteins such as p-Rb, cyclin D1 and p27, as well as apoptotic proteins such as Bax, Bcl-2, caspase-3, and poly (ADP-ribose) polymerase (PARP). , coadministration with Lpz and Gef significantly attenuated the growth of A549 nude mouse xenograft models. These findings suggest that Lpz might be applied in combination with Gef for NSCLC therapy, but further evidence is required.
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http://dx.doi.org/10.3389/fcell.2021.655559DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8093516PMC
April 2021

Targeting c-Jun in A549 Cancer Cells Exhibits Antiangiogenic Activity and Through Exosome/miRNA-494-3p/PTEN Signal Pathway.

Front Oncol 2021 9;11:663183. Epub 2021 Apr 9.

Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin, China.

The oncogene c-Jun is activated by Jun N-terminal kinase (JNK). Exosomes are nanometer-sized membrane vesicles released from a variety of cell types, and are essential for cell-to-cell communication. By using specific JNK inhibitor SP600125 or CRISPR/Cas9 to delete c-Jun, we found that exosomes from SP600125-treated A549 cancer cells (Exo-SP) or from c-Jun-KO-A549 cells (Exo-c-Jun-KO) dramatically inhibited tube formation of HUVECs. And the miR-494 levels in SP600125 treated or c-Jun-KO A549 cells, Exo-SP or Exo-c-Jun-KO, and HUVECs treated with Exo-SP or Exo-c-Jun-KO were significantly decreased. Meanwhile, Exo-SP and Exo-c-Jun-KO enhanced expression of phosphatase and tensin homolog deleted on chromosome ten (PTEN). Addition of miR-494 agomir in Exo-c-Jun-KO treated HUVECs inhibited PTEN expression and promoted tube formation, suggesting the target of miR-494 might be PTEN in HUVECs. Moreover, A549 tumor xenograft model and Matrigel plug assay demonstrated that Exo-c-Jun-KO attenuated tumor growth and angiogenesis through reducing miR-494. Taken together, inhibition of c-Jun in A549 cancer cells exhibited antiangiogenic activity and through exosome/miRNA-494-3p/PTEN signal pathway.
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http://dx.doi.org/10.3389/fonc.2021.663183DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8062808PMC
April 2021

Daytime, Not Nighttime, Elevated Atmospheric Carbon Dioxide Exposure Improves Plant Growth and Leaf Quality of Mulberry ( L.) Seedlings.

Front Plant Sci 2020 4;11:609031. Epub 2021 Feb 4.

Centre of Excellence for Soil Biology, School of Resource and Environment, Southwest University, Chongqing, China.

Almost all elevated atmospheric CO concentrations (eCO) studies have not addressed the potential responses of plant growth to different CO in daytime and nighttime. The present study was to determine the impact of daytime and/or nighttime eCO on growth and quality of mulberry ( L.), a perennial multipurpose cash plant. Six-month-old mulberry seedlings were hence grown in environmentally auto-controlled growth chambers under four CO concentrations: (1) ambient CO (ACO, 410 μmol mol daytime/460 μmol mol nighttime), (2) sole daytime elevated CO (DeCO, 710 μmol mol/460 μmol mol), (3) sole nighttime elevated CO (NeCO, 410 μmol mol/760 μmol mol), and (4) continuous daytime and nighttime elevated CO (D + NeCO, 710 μmol mol/760 μmol mol). Plant growth characteristics, nutrient uptake, and leaf quality were then examined after 120 days of CO exposure. Compared to control, DeCO and (D + N)eCO increased plant biomass production and thus the harvest of nutrients and accumulation of leaf carbohydrates (starch, soluble sugar, and fatty acid) and N-containing compounds (free amino acid and protein), though there were some decreases in the concentration of leaf N, P, Mg, Fe, and Zn. NeCO had no significant effects on leaf yield but an extent positive effect on leaf nutritional quality due to their concentration increase in leaf B, Cu, starch, and soluble sugar. Meanwhile, (D + N)eCO decreased mulberry leaf yield and harvest of nutritious compounds for silkworm when compared with DeCO. The reason may be associated to N, P, Mg, Fe, and Zn that are closely related to leaf pigment and N metabolism. Therefore, the rational application of mineral nutrient (especially N, P, Fe, Mg, and Zn) fertilizers is important for a sustainable mulberry production under future atmosphere CO concentrations.
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http://dx.doi.org/10.3389/fpls.2020.609031DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7890035PMC
February 2021

STIM1 promotes angiogenesis by reducing exosomal miR-145 in breast cancer MDA-MB-231 cells.

Cell Death Dis 2021 01 4;12(1):38. Epub 2021 Jan 4.

Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, 300070, Tianjin, China.

Cancer cells secrete abundant exosomes, and the secretion can be promoted by an increase of intracellular Ca. Stromal interaction molecule 1 (STIM1) plays a key role in shaping Ca signals. MicroRNAs (miRNAs) have been reported to be potential therapeutic targets for many diseases, including breast cancer. Recently, we investigated the effect of exosomes from STIM1-knockout breast cancer MDA-MB-231 cells (Exo-STIM1-KO), and from SKF96365-treated MDA-MB-231 cells (Exo-SKF) on angiogenesis in human umbilical vein endothelial cells (HUVECs) and nude mice. The exosomes Exo-STIM1-KO and Exo-SKF inhibited tube formation by HUVECs remarkably. The miR-145 was increased in SKF96365 treated or STIM1-knockout MDA-MB-231 cells, Exo-SKF and Exo-STIM1-KO, and HUVECs treated with Exo-SKF or Exo-STIM1-KO. Moreover, the expressions of insulin receptor substrate 1 (IRS1), which is the target of miR-145, and the downstream proteins such as Akt/mammalian target of rapamycin (mTOR), Raf/extracellular signal regulated-protein kinase (ERK), and p38 were markedly inhibited in HUVECs treated with Exo-SKF or Exo-STIM1-KO. Matrigel plug assay in vivo showed that tumor angiogenesis was suppressed in Exo-STIM1-KO, but promoted when miR-145 antagomir was added. Taken together, our findings suggest that STIM1 promotes angiogenesis by reducing exosomal miR-145 in breast cancer MDA-MB-231 cells.
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http://dx.doi.org/10.1038/s41419-020-03304-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7791041PMC
January 2021

HTBPI, an active phenanthroindolizidine alkaloid, inhibits liver tumorigenesis by targeting Akt.

FASEB J 2020 09 24;34(9):12255-12268. Epub 2020 Jul 24.

Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

Akt, a crucial protein involved in a variety of signaling pathways in cancer, acts as an important regulator of survival in hepatocellular carcinoma (HCC), and provides curative option for the related drugs development. We have found an active phenanthroindolizidine alkaloid, (13aR,14R)-9,11,12,13,13a,14-hexahydro-3,6,7-trimethoxydibenzo[f,h]pyrrolo[1,2-b]isoquinolin-14-ol (HTBPI), is a promising Akt inhibitor effective in the suppression of HCC cells proliferation through stimulating apoptotic and autophagic capability in vivo and in vitro. Treatment of HTBPI combined with a classical autophagy-lysosomal inhibitor (bafilomycin A1), could enhance stimulation effects of apoptosis on HCC cell lines. In addition, we confirmed HTBPI targeting Akt, occupied the kinase binding domain (Thr 308) of Akt to inactivate its function by CETSA and DARTS assay. In contrast, ectopic Akt-induced overexpression significantly abrogated inhibitory effects of HTBPI on cell viability and proliferation. Furthermore, high p-Akt (Thr 308) expression is collated with liver tumor formation and poor survival in HCC patients. In conclusions, HTBPI impeded HCC progress through regulation of apoptosis and autophagy machinery via interaction with p-Akt (Thr 308). This may provide potential molecular candidate by targeting Akt for the therapy of HCC patients.
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http://dx.doi.org/10.1096/fj.202000254RDOI Listing
September 2020

Anticancer activities of TCM and their active components against tumor metastasis.

Biomed Pharmacother 2021 Jan 11;133:111044. Epub 2020 Dec 11.

State Key Laboratory of Component-based Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China. Electronic address:

Traditional Chinese Medicine (TCM) has the characteristics of multiple targets, slight side effects and good therapeutic effects. Good anti-tumor effects are shown by Traditional Chinese Medicine prescription, Chinese patent medicine, single Traditional Chinese Medicine and Traditional Chinese medicine monomer compound. Clinically, TCM prolonged the survival time of patients and improved the life quality of patients, due to less side effects. Cancer metastasis is a complex process involving numerous steps, multiple genes and their products. During the process of tumor metastasis, firstly, cancer cell increases its proliferative capacity by reducing autophagy and apoptosis, and then the cancer cell capacity is stimulated by increasing the ability of tumors to absorb nutrients from the outside through angiogenesis. Both of the two steps can increase tumor migration and invasion. Finally, the purpose of tumor metastasis is achieved. By inhibiting autophagy and apoptosis of tumor cells, angiogenesis and EMT outside the tumor can inhibit the invasion and migration of cancer, and consequently achieve the purpose of inhibiting tumor metastasis. This review explores the research achievements of Traditional Chinese Medicine on breast cancer, lung cancer, hepatic carcinoma, colorectal cancer, gastric cancer and other cancer metastasis in the past five years, summarizes the development direction of TCM on cancer metastasis research in the past five years and makes a prospect for the future.
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http://dx.doi.org/10.1016/j.biopha.2020.111044DOI Listing
January 2021

Compound Heterozygosity for a Novel Mutation Codon 104 (-A) (: c.313delA) and Codons 41/42 (-CTTT) (: c.126_129delCTTT) Leading to β-Thalassemia Major in a Chinese Family.

Hemoglobin 2020 Nov 16;44(6):402-405. Epub 2020 Nov 16.

Department of Clinical Laboratory, First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, People's Republic of China.

β-Thalassemia (β-thal) is a hereditary blood disorder characterized by the reduced or absent synthesis of β-globin chains. Here, we report a case of severe thalassemia with compound heterozygosity for a novel deletion mutation at codon 104 (-A) (: c.313delA) and codons 41/42 (-CTTT) (: c.126_129delCTTT) on the β-globin gene (), and a coinheritance of the -α (leftward) deletion on the α-globin gene cluster. The proband was a 12-year-old boy, and four other family members were involved in this study. This novel frameshift mutation caused classical β-thal trait in the heterozygote and a transfusion-dependent form of β-thal major (β-TM) in compound heterozygosity with other β mutations.
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http://dx.doi.org/10.1080/03630269.2020.1843482DOI Listing
November 2020

TPPP3 Associated with Prognosis and Immune Infiltrates in Head and Neck Squamous Carcinoma.

Biomed Res Int 2020 6;2020:3962146. Epub 2020 Oct 6.

Department of Clinical Laboratory, First Affiliated Hospital Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China.

Tubulin polymerization promoting protein family member 3 (TPPP3) is a kind of protein that can mediate the dynamics and stability of microtubules. However, the correlations of TPPP3 between prognosis and immune infiltrates in different tumors are still unclear. The analysis of TPPP3 expression was performed via Oncomine and Gene Expression Profiling Interactive Analysis (GEPIA) website. We also used GEPIA to assess the impact of TPPPT3 on clinical outcomes. The related pathways involved in TPPP3 were analyzed by gene-set enrichment analysis (GSEA), and the correlation between TPPP3 and immune infiltration was studied by Tumor Immune Estimation Resource2.0 (TIMER 2.0). The TPPP3 expression was significantly reduced in head and neck squamous carcinoma (HNSC) compared to adjacent tissues. In addition, the low expression of TPPP3 in HNSC was significantly associated with prognosis. The pathways closely related to the low expression of TPPP3 are "Antigen Processing and Presentation," "Primary Immunodeficiency," and so on. The TPPP3 expression was negatively correlated with the level of CD8+ T cell, B cell, and myeloid dendritic cell infiltration in HNSC. The TPPP3 expression is closely related to multiple immunomarkers in CD8+ T cell and Myeloid dendritic cells. These data indicate that TPPP3 is associated with multiple cancers and involves multiple immune-related pathways, and TPPP3 is associated with immune infiltration levels. Besides, the TPPP3 expression may help regulate tumor-associated CD8 + T cells, DC cells in HNSC. We conclude TPPP3 can be considered as a biomarker for predicting head and neck squamous cell carcinoma prognosis and immune infiltration.
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http://dx.doi.org/10.1155/2020/3962146DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7563072PMC
May 2021

Cellular senescence and cancer: Focusing on traditional Chinese medicine and natural products.

Cell Prolif 2020 Oct 3;53(10):e12894. Epub 2020 Sep 3.

Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

Cancer is the principal cause of death and a dominant public health problem which seriously threatening human life. Among various ways to treat cancer, traditional Chinese medicine (TCM) and natural products have outstanding anti-cancer effects with their unique advantages of high efficiency and minimal side effects. Cell senescence is a physiological process of cell growth stagnation triggered by stress, which is an important line of defence against tumour development. In recent years, active ingredients of TCM and natural products, as an interesting research hotspot, can induce cell senescence to suppress the occurrence and development of tumours, by inhibiting telomerase activity, triggering DNA damage, inducing SASP, and activating or inactivating oncogenes. In this paper, the recent research progress on the main compounds derived from TCM and natural products that play anti-cancer roles by inducing cell senescence is systematically reviewed, aiming to provide a reference for the clinical treatment of pro-senescent cancer.
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http://dx.doi.org/10.1111/cpr.12894DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7574878PMC
October 2020

Effect of Different Expression of Immune-Related lncRNA on Colon Adenocarcinoma and Its Relation to Prognosis.

Biomed Res Int 2020 6;2020:6942740. Epub 2020 Jun 6.

Department of Clinical Laboratory, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China.

Objective: To explore the expression of immune-related lncRNAs in colon adenocarcinoma and find out the effect on how these lncRNAs influence the development and prognosis of colon adenocarcinoma.

Method: Transcriptome data of colon adenocarcinoma from The Cancer Genome Atlas (TCGA) were downloaded, and gene sets "IMMUNE RESPONSE" and "IMMUNE SYSTEM PROCESS" were sought from the Molecular Signatures Database (MSigDB). The expression of immune-related genes was extracted that were immune-related mRNAs. Then, the immune-related lncRNAs were sought out by utilizing of the above data. Clinical traits were combined with immune-related lncRNAs, so that prognostic-related lncRNAs were identified by Cox regression. Multivariate Cox regression was built to calculate risk scores. Relationships between clinical traits and immune-related lncRNAs were also calculated.

Result: A total of 480 colorectal adenocarcinoma patients and 41 normal control patients' transcriptome sequencing data of tissue samples were obtained from TCGA database. 918 immune-related lncRNAs were screened. Cox regression showed that 34 immune-related lncRNAs were associated with colon adenocarcinoma prognosis. Seven lncRNAs were independent risk factors.

Conclusion: This study revealed that some lncRNAs can affect the development and prognosis of colon adenocarcinoma. It may provide new theory evidence of molecular mechanism for the future research and molecular targeted therapy of colon adenocarcinoma.
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http://dx.doi.org/10.1155/2020/6942740DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7294360PMC
March 2021

Identification of Prognostic Immune Genes in Bladder Urothelial Carcinoma.

Biomed Res Int 2020 20;2020:7510120. Epub 2020 Jan 20.

Department of Clinical Laboratory, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China.

Background: The aim of this study is to identify possible prognostic-related immune genes in bladder urothelial carcinoma and to try to predict the prognosis of bladder urothelial carcinoma based on these genes.

Methods: The Cancer Genome Atlas (TCGA) expression profile data and corresponding clinical traits were obtained. Differential gene analysis was performed using R software. Reactome was used to analyze the pathway of immune gene participation. The differentially expressed transcription factors and differentially expressed immune-related genes were extracted from the obtained list of differentially expressed genes, and the transcription factor-immune gene network was constructed. To analyze the relationship between immune genes and clinical traits of bladder urothelial carcinoma, a multifactor Cox proportional hazards regression model based on the expression of immune genes was established and validated.

Results: Fifty-eight immune genes were identified to be associated with the prognosis of bladder urothelial carcinoma. These genes were enriched in Cytokine Signaling in Immune System, Signaling by Receptor Tyrosine Kinases, Interferon alpha/beta signaling, and other immune related pathways. Transcription factor-immune gene regulatory network was established, and EBF1, IRF4, SOX17, MEF2C, NFATC1, STAT1, ANXA6, SLIT2, and IGF1 were screened as hub genes in the network. The model calculated by the expression of 16 immune genes showed a good survival prediction ability ( < 0.05 and AUC = 0.778).

Conclusion: A transcription factor-immune gene regulatory network related to the prognosis of bladder urothelial carcinoma was established. EBF1, IRF4, SOX17, MEF2C, NFATC1, STAT1, ANXA6, SLIT2, and IGF1 were identified as hub genes in the network. The proportional hazards regression model constructed by 16 immune genes shows a good predictive ability for the prognosis of bladder urothelial carcinoma.
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http://dx.doi.org/10.1155/2020/7510120DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7201587PMC
February 2021

Corrigendum: DT-13 Inhibits Proliferation and Metastasis of Human Prostate Cancer Cells Through Blocking PI3K/Akt Pathway.

Front Pharmacol 2020 8;11:462. Epub 2020 Apr 8.

Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin, China.

[This corrects the article DOI: 10.3389/fphar.2018.01450.].
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http://dx.doi.org/10.3389/fphar.2020.00462DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7159031PMC
April 2020

Identification of Genes Associated with the Metastasis of Pheochromocytoma/Paraganglioma Based on Weighted Gene Coexpression Network Analysis.

Biomed Res Int 2020 5;2020:3876834. Epub 2020 Feb 5.

Department of Clinical Laboratory, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China.

Background: Pheochromocytoma/paraganglioma (PCPG) is a benign neuroendocrine neoplasm in most cases, but metastasis and other malignant behaviors can be observed in this tumor. The aim of this study was to identify genes associated with the metastasis of PCPG.

Methods: The Cancer Genome Atlas (TCGA) expression profile data and clinical information were downloaded from the cbioportal, and the weighted gene coexpression network analysis (WGCNA) was conducted. The gene coexpression modules were extracted from the network through the WGCNA package of R software. We further extracted metastasis-related modules of PCPG. Enrichment analysis of Biological Process of Gene Ontology and Kyoto Encyclopedia of Genes and Genomes was carried out for important modules, and survival analysis of hub genes in the modules was performed.

Results: A total of 168 PCPG samples were included in this study. The weighted gene coexpression network was constructed with 5125 genes of the top 25% variance among the 20501 genes obtained from the database. We identified 11 coexpression modules, among which the salmon module was associated with the age of PCPG patients at diagnosis, metastasis, and malignancy of the tumors.

Conclusion: WGCNA was performed to identify the gene coexpression modules and hub genes in the metastasis-related gene module of PCPG. The findings in this study provide a new clue for further study of the mechanisms underlying the PCPG metastasis.
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http://dx.doi.org/10.1155/2020/3876834DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7025031PMC
November 2020

Diagnostic value of hemoglobin and neutrophil-to-lymphocyte ratio in Behcet Disease.

Medicine (Baltimore) 2019 Dec;98(52):e18443

Department of Clinical Laboratory. First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi Zhuang Autonomous Region, China.

The purpose of our study was to investigate the diagnostic value of NLR, hemoglobin (HB) and combine NLR with HB in the BD patients.Sixty-seven patients with BD were diagnosed in the rheumatology or dermatology between June 2015 and June 2019; 92 matching healthy physical examiners were included in our study. SPSS was used for statistical analysis.Compared with the healthy control, NLR was increased (P < .001), while the HB level was decreased (P < .001) in the patients of BD. In addition, ESR and CRP were increased in BD patients. NLR has no relationship with CRP and ESR, while the HB levels were negatively correlated with CRP and ESR (r = -0.293, P = .046; r = -0.431, P = .002). ROC curve analysis revealed the AUC of NLR and HB were 0.797 and 0.798 (P < .001). When combined NLR with HB, the AUC was 0.897 (P < .001). Besides, logistic regression analysis demonstrated that NLR and HB were independent risk factors in the BD patients.We observed that the diagnostic value of NLR, HB and combined NLR with HB in the BD patients were high, particularly when combine NLR with HB. NLR and HB were independent risk factors in the BD patients. In addition, HB levels related to the disease activity of BD patients.
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http://dx.doi.org/10.1097/MD.0000000000018443DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6946511PMC
December 2019

Clinical significance of serum bilirubin in primary Sjögren syndrome patients.

J Clin Lab Anal 2020 Mar 6;34(3):e23090. Epub 2019 Nov 6.

Department of Clinical Laboratory, First Affiliated Hospital of Guangxi Medical University, Nanning, China.

Objective: The purpose of our research was to demonstrate the clinical significance of serum bilirubin in primary Sjögren syndrome patients (pSS).

Patients And Methods: A total of 116 patients with primary Sjögren syndrome and 138 matched individuals were included in our study. The laboratory parameters of patients with pSS and healthy controls were retrospectively analyzed.

Results: Serum total bilirubin, direct bilirubin, and indirect bilirubin were significantly reduced (P < .001, P = .001, P < .001) while ESR was significantly increased (P < .001) in patients with pSS when compared with healthy checkup individuals. Statistically, the AUC in patients with pSS is as follows: TBIL = 0.77, P < .001, cutoff value = 7.96; DBIL = 0.617, P = .001 cutoff value = 2.2; and IBIL = 0.786, P < .001 cutoff value = 4.5. Furthermore, our study revealed that TBIL, DBIL, and IBIL were significantly negativity related to ESR (r = -.406, P < .001; r = -.206, P = .026; r = -.429, P < .001). Interestingly, multiple linear regression analysis showed that when adjusted for sex, age, ALT, and AST, the levels of TBIL, DBIL, and IBIL in patients with pSS were independently correlated with ESR.

Conclusions: This study found that the levels of serum bilirubin were reduced and the inflammatory marker was elevated in patients with pSS. Additionally, serum bilirubin was negatively related with ESR and TBIL, DBIL, and IBIL can be used in the clinical diagnosis and follow-up visits of the patients with pSS.
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http://dx.doi.org/10.1002/jcla.23090DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7083477PMC
March 2020

Alkaloids from Traditional Chinese Medicine against hepatocellular carcinoma.

Biomed Pharmacother 2019 Dec 23;120:109543. Epub 2019 Oct 23.

Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, China. Electronic address:

Hepatocellular carcinoma (HCC) has become one of the major diseases that are threatening human health in the 21st century. Currently there are many approaches to treat liver cancer, but each has its own advantages and disadvantages. Among various methods of treating liver cancer, natural medicine treatment has achieved promising results because of their superiorities of high efficiency and availability, as well as low side effects. Alkaloids, as a class of natural ingredients derived from traditional Chinese medicines, have previously been shown to exert prominent anti-hepatocarcinogenic effects, through various mechanisms including inhibition of proliferation, metastasis and angiogenesis, changing cell morphology, promoting apoptosis and autophagy, triggering cell cycle arrest, regulating various cancer-related genes as well as pathways and so on. As a consequence, alkaloids suppress the development and progression of liver cancer. In this study, the mechanisms of representative alkaloids against hepatocarcinoma in each class are described systematically according to the structure classification, which mainly divides alkaloids into piperidine alkaloids, isoquinoline alkaloids, indole alkaloids, terpenoids alkaloids, steroidal alkaloids and other alkaloids. Besides using them alone, synergistic effects created together with other chemotherapy drugs and some special preparation methods also have been demonstrated. In this review, we have summarized the potential roles of several common alkaloids in the prevention and treatment of HCC, by revising the preclinical studies, highlighting the potential applications of alkaloids when they function as a therapeutic choice for HCC treatment, and integrating them into clinical practices.
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http://dx.doi.org/10.1016/j.biopha.2019.109543DOI Listing
December 2019

Atorvastatin Exerts Antileukemia Activity via Inhibiting Mevalonate-YAP Axis in K562 and HL60 Cells.

Front Oncol 2019 9;9:1032. Epub 2019 Oct 9.

Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin, China.

Novel therapeutic strategies are still urgently expected for leukemia despite undisputed success of various targeted therapeutics. The antileukemia activity of Atorvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on human leukemia cells was investigated. Atorvastatin inhibited K562 and HL60 cell proliferation, induced G2/M cell cycle arrest in K562 cells by down-regulating cyclinB1 and cdc2, but G0/G1 arrest in HL60 cells by up-regulating p27 and down-regulating cyclinD1 and p-pRb. Atorvastatin also induced apoptosis in both cell lines, in which the reactive oxygen species (ROS)-related mitochondrial apoptotic signaling might be involved, with increase of ROS and Bax/Bcl-2 ratio, loss of mitochondrial membrane potential (MMP), release of cytochrome C into cytosol, and activation of Bax/Caspase-9/Caspase-3/PARP pathway. Inhibition of YAP nuclear localization and activation by Atorvastatin was reversed by the addition of mevalonate, GGPP, or FPP. Further, the effects on cell cycle arrest- and apoptosis- related proteins by Atorvastatin were alleviated by addition of mevalonate, suggesting the antileukemia effect of Atorvastatin might be through mevalonate-YAP axis in K562 and HL60 cells. Our results suggest that Atorvastatin might be used for leukemia therapy while evidence of clinical efficacy is required.
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http://dx.doi.org/10.3389/fonc.2019.01032DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6794561PMC
October 2019

Co-targeting PI3K/Akt and MAPK/ERK pathways leads to an enhanced antitumor effect on human hypopharyngeal squamous cell carcinoma.

J Cancer Res Clin Oncol 2019 Dec 16;145(12):2921-2936. Epub 2019 Oct 16.

Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, 300070, Tianjin, China.

Purpose: The present study aims to determine whether co-targeting PI3K/Akt and MAPK/ERK pathways in human hypopharyngeal squamous cell carcinoma (HSCC) is a potential anticancer strategy.

Methods: We retrospectively analyzed the clinical data of HSCC patients, and the phosphorylation status of Akt and Erk in HSCC and tumor adjacent tissues was evaluated by immunohistochemistry. MTT and colony formation assay were performed to determine the anti-proliferative effect of PI3K/mTOR inhibitor GDC-0980 and MEK inhibitor Refametinib on HSCC cell line Fadu. Wound-healing and Transwell migration assay were used to analyze the anti-migrative capability of the two drugs. The involved anti-tumor mechanism was explored by flow cytometry, qRT-PCR and western blot. The combinational anticancer effect of GDC-0980 and Refametinib was evaluated according to Chou and Talalay's method.

Results: The levels of p-Akt and p-Erk were increased significantly with the progression of clinical stage of HSCC, suggesting PI3K/Akt and MAPK/ERK pathways might be associated with HSCC occurrence and progression. Furthermore, both GDC-0980 and Refametinib showed obvious antitumor effects on FaDu cells. Treatment by the two drugs arrested FaDu cell cycle progression in G1 phase, with reduction of cyclin D1 and p-Rb, in contrast to enhancement of p27. GDC-0980 inhibited FaDu cell migration and reduced metastasis related proteins including p-PKCζ, p-Integrin β1 and uPA. Combination use of GDC-0980 and Refametinib exhibited strong synergistic anti-tumor effect.

Conclusion: Dual inhibition of PI3K/Akt and MAPK/ERK pathway by GDC-0980 and Refametinib might be a promising treatment strategy for HSCC patients.
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http://dx.doi.org/10.1007/s00432-019-03047-2DOI Listing
December 2019

Sophoridine Inhibits Human Colorectal Cancer Progression via Targeting MAPKAPK2.

Mol Cancer Res 2019 12 1;17(12):2469-2479. Epub 2019 Oct 1.

Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

is a traditional Chinese medicine commonly used to treat cancer in China. However, its active components and underlying mechanism remain ambiguous. In this study, we have screened the pharmacokinetic parameters of the main chemical constituents of by Traditional Chinese Medicine Systems Pharmacology (TCMSP) Database and Analysis Platform and have found that Sophoridine is one of the best antitumor active ingredients. We have found that MAPKAPK2 is a potential target for Sophoridine by the PharmMapper and KEGG databXase analysis. Moreover, we have found that Sophoridine selectively inactivates phospho-MAPKAPK2 (Thr222) and directly binds into the ATP site of MAPKAPK2 by molecular docking. Furthermore, we have found out a direct binding between MAPKAPK2 and Sophoridine by cellular thermal shift assay and drug affinity responsive targets stability assay. The inhibition effects are further confirmed by Western blot: Sophoridine significantly decreases phospho-MAPKAPK2 (Thr222) in a time-dependent manner, but there is no obvious change in its total expression in colorectal cancer cells. Clinical studies have shown that a higher level of MAPKAPK2 is associated with a poorer percent survival rate (prognosis). Furthermore, a higher level of MAPKAPK2 is positively associated with the enrichment of downregulation of apoptosis and autophagy by gene set enrichment analysis, as well as upregulation of proliferation and cell-cycle arrest. Taken together, our results suggest that the MAPKAPK2 plays a key role in Sophoridine-inhibited growth and invasion in colorectal cancers. IMPLICATIONS: These studies show that Sophoridine may be a promising therapeutic strategy that blocks tumorigenesis in colorectal cancers.
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http://dx.doi.org/10.1158/1541-7786.MCR-19-0553DOI Listing
December 2019

7-Deoxynarciclasine shows promising antitumor efficacy by targeting Akt against hepatocellular carcinoma.

Int J Cancer 2019 12 23;145(12):3334-3346. Epub 2019 May 23.

Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

Akt is a promising therapeutic target for cancer treatment. In our study, we have identified that 7-deoxynarciclasine (7-DONCS) is a potential inhibitor of Akt, which results in the repression of multiple oncogenic processes in hepatocellular carcinoma (HCC). We have found that 7-DONCS suppresses the growth of HCC by inducing the apoptotic and autophagic capacities, as well as by inhibiting epithelial-mesenchymal transition (EMT) in vitro and in vivo. Pretreatment of cells with specific autophagy inhibitor (Bafilomycin A1) or knockdown of endogenous LC‐3B by siRNA strongly enhences 7‐DONCS‐regulated apoptosis and EMT. Consequently, we have found that 7-DONCS selectively inhibits phospho-Akt (Ser473), and subsequent molecular docking reveals that 7-DONCS directly binds to the C-terminal domain of Akt. Overexpressing Akt significantly blocks these effects via 7-DONCS in HCC cells. Furthermore, 7-DONCS, by targeting Akt, exhibits a promising therapeutic effect in orthotopic hepatocellular tumors. Finally, higher p-Akt expression is associated with poor prognosis, and higher level of Akt was positively correlated with the enrichment of both apoptosis and autophagy downregulation, and EMT upregulation in HCC patients. These studies suggest that 7-DONCS serves as an attractive drug candidate by targeting Akt for future HCC therapy.
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http://dx.doi.org/10.1002/ijc.32395DOI Listing
December 2019

Blood cell parameters for screening and diagnosis of hereditary spherocytosis.

J Clin Lab Anal 2019 May 3;33(4):e22844. Epub 2019 Apr 3.

Department of Clinical Laboratory, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.

Background: There is currently no single index for the diagnostic screening of hereditary spherocytosis (HS). However, hematology analyzers are widely used in hospital laboratories because of their highly automated performance and quality control procedure, and detection of some blood cell parameters may be useful for the early screening of HS.

Methods: We investigated the values of blood cell parameters for the screening and differential diagnosis of HS. We performed a descriptive study of 482 samples (67 cases of HS, 59 cases of G6PD deficiency, 57 cases of AIHA, 199 cases of thalassemia, and 100 cases of healthy controls) that were run on Beckman Coulter LH780 Hematology Analyzer.

Results: HS was characterized by increased MCHC, decreased MRV, MSCV-MCV < 0, and increased Ret with no concomitant increase in IRF. The areas under the ROC curves were MSCV-MCV (0.97; 95% CI 0.95-1.0) > MRV (0.94; 95% CI 0.91-0.97) > MCHC (0.92; 95% CI 0.88-0.97) > Ret/IRF (0.77; 95% CI 0.7-0.84). MSCV-MCV ≤ 0.6 fl was valuable parameter for the diagnostic screening of HS, with a sensitivity of 95.5% and specificity of 94.9%.

Conclusion: These indices have high reference values for differentiating HS from thalassemia, AIHA, and G6PD deficiency.
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http://dx.doi.org/10.1002/jcla.22844DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6528600PMC
May 2019

Inhibitory effect of taxifolin on mast cell activation and mast cell-mediated allergic inflammatory response.

Int Immunopharmacol 2019 Jun 26;71:205-214. Epub 2019 Mar 26.

Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China; Research Center, School of Medicine, Tianjin Tianshi College, Tianyuan University, Tianjin 301700, China. Electronic address:

The aim of the present study is to investigate the anti-inflammatory and anti-allergic effects of taxifolin on mast cells and mast cell-mediated allergic reaction. We assessed the effect of taxifolin on the activation of bone marrow-derived mast cells (BMMCs) and rat basophilic leukemia (RBL)-2H3 cells induced by immunoglobulin E (IgE)/antigen (Ag), and the activation of human mast cell line (HMC-1) induced by PMA plus A23187. Taxifolin inhibited degranulation, generation of leukotriene C (LTC), production of interlukin-6 (IL-6), and expression of cyclooxygenase-2 (COX-2) through blocking intracellular Ca mobilization, phosphorylation of phospholipase Cγ (PLCγ) and mitogen-activated protein kinases (MAPKs), translocation of cytosolic phospholipase A (cPLA) and 5-lipoxygenase (5-LO), and Akt/IKK/NF-κB pathway, in BMMC cells. Furthermore, taxifolin suppressed phosphorylation of Syk, but without effect on Fyn and Lyn. Taxifolin also inhibited activation of RBL-2H3 and HMC-1 cells via Akt/IKK/NF-κB and MAPKs/cPLA signal pathway. Treatment with taxifolin attenuated the mast cell-mediated passive cutaneous anaphylaxis (PCA) reaction. Our results suggest that taxifolin might become a potential drug candidate for the treatment of allergic and inflammatory diseases.
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http://dx.doi.org/10.1016/j.intimp.2019.03.038DOI Listing
June 2019

DT-13 Inhibits Proliferation and Metastasis of Human Prostate Cancer Cells Through Blocking PI3K/Akt Pathway.

Front Pharmacol 2018 7;9:1450. Epub 2018 Dec 7.

Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin, China.

DT-13, a saponin monomer 13 from the dwarf lilyturf tuber, was reported to exhibit anti-inflammatory, hepatoprotective, cardioprotective as well as antitumor activities in a number of tumor cells. Prostate cancer is the second leading cause of cancer death in males, discovery of novel antitumor drug for therapy of prostate cancer is expected. Aiming to evaluate whether DT-13 could become a candidate to treat prostate cancer, we recently investigated the antitumor effect of DT-13 on human prostate cancer cells and the underlying mechanism. DT-13 was found to effectively inhibit proliferation and metastasis of prostate cancer PC3 and DU145 cell lines in a dose-dependent manner. Treatment by DT-13 resulted in a mitochondria-mediated apoptosis, which was accompanied by the chromatin condensation and nuclear shrinkage in the prostate cancer cells. Moreover, DT-13 caused remarkable upregulation of Bax, Bad, Cytochrome C, cleaved -caspase 3, -caspase 9 and -PARP, in contrast to the downregulation of Bcl-2. Nevertheless, no obvious change in intracellular ROS level was observed after DT-13 treatment. We further demonstrated that DT-13 could inhibit PC3 cell metastasis in which suppression of Integrinβ1 and MMP2/9 might be involved. Western blot analysis indicated DT-13 significantly decreased the phosphorylation of PDK1, Akt, mTOR as well as p70S6K, suggesting the pro-apoptotic and anti-metastatic effects of DT-13 on prostate cancer cells might be attributed to the blockade of PI3K/Akt pathway. Collectively, our findings suggest DT-13 is worthy of further investigation as a drug candidate for the treatment of prostate cancer.
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http://dx.doi.org/10.3389/fphar.2018.01450DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6292965PMC
December 2018

Alisol B 23-Acetate Inhibits IgE/Ag-Mediated Mast Cell Activation and Allergic Reaction.

Int J Mol Sci 2018 Dec 18;19(12). Epub 2018 Dec 18.

Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China.

Alisol B 23-acetate (AB23A), a natural triterpenoid, has been reported to exert hepatoprotective and antitumor activities. Aiming to investigate the anti-inflammatory activity, this study examined the effect of AB23A on mast cells and allergic reaction. AB23A inhibited the degranulation of mast cells stimulated by immunoglobulin E/antigen (IgE/Ag), and also decreased the synthesis of leukotriene C₄ (LTC₄), production of interlukin-6 (IL-6), and expression of cyclooxygenase-2 (COX-2) in a concentration-dependent manner with no significant cytotoxicity in bone marrow-derived mast cells (BMMCs). AB23A inhibited spleen tyrosine kinase (Syk) and the downstream signaling molecules including phospholipase Cγ (PLCγ), serine-threonine protein kinase/inhibitor of nuclear factor kappa-B kinase/nuclear factor kappa-B (Akt/IKK/NF-κB), and mitogen-activated protein kinases/cytosolic phospholipase A₂ (MAPK/cPLA₂). Furthermore, AB23A blocked mobilization of Ca. Similar results were obtained in other mast cell lines Rat basophilic leukemia (RBL)-2H3 cells and a human mast cell line (HMC-1). In addition, AB23A attenuated allergic responses in an acute allergy animal model, passive cutaneous anaphylaxis (PCA). Taken together, this study suggests that AB23A inhibits the activation of mast cells and ameliorates allergic reaction, and may become a lead compound for the treatment of mast cell-mediated allergic diseases.
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http://dx.doi.org/10.3390/ijms19124092DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6320761PMC
December 2018

Lycorine Displays Potent Antitumor Efficacy in Colon Carcinoma by Targeting STAT3.

Front Pharmacol 2018 8;9:881. Epub 2018 Aug 8.

Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

Signal transducer and activator of transcription 3 (STAT3) is an attractive therapeutic target for cancer treatment. In this study, we identify lycorine is an effective inhibitor of STAT3, leading to repression of multiple oncogenic processes in colon carcinoma. Lycorine selectively inactivates phospho-STAT3 (Tyr-705), and subsequent molecular docking uncovers that lycorine directly binds to the SH2 domain of STAT3. Consequently, we find that lycorine exhibits anti-proliferative activity and induces cell apoptosis on human colorectal cancer (CRC) . Lycorine induces the activation of the caspase-dependent mitochondrial apoptotic pathway, as indicated by activation of caspase and increase of the ratio of Bax/Bcl-2 and mitochondrial depolarization. Overexpressing STAT3 greatly blocks these effects by lycorine in CRC cells. Finally, lycorine exhibits a potential therapeutic effect in xenograft colorectal tumors by targeting STAT3 without observed toxicity. Taken together, the present study indicates that lycorine acts as a promising inhibitor of STAT3, which blocks tumorigenesis in colon carcinoma.
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http://dx.doi.org/10.3389/fphar.2018.00881DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6092588PMC
August 2018

Spinacetin Suppresses the Mast Cell Activation and Passive Cutaneous Anaphylaxis in Mouse Model.

Front Pharmacol 2018 30;9:824. Epub 2018 Jul 30.

Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin, China.

We previously reported the anti-inflammatory and anti-asthmatic activities of the extract of the Thunb. Aiming for discovery of a novel anti-inflammatory compound, we isolated spinacetin from the extract and investigated its and anti-inflammatory effect and the related mechanism. Effect of spinacetin on the Syk signaling pathway was studied in bone marrow-derived mast cells (BMMCs), and that on the nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs) was investigated in Rat basophilic leukemia (RBL)-2H3 cells and human mast cell line (HMC-1). The anti-inflammatory activity was assessed with passive cutaneous anaphylaxis (PCA) reaction assay. Spinacetin significantly inhibited the release of histamine, and production of inflammatory mediators such as leukotriene C (LTC) and interlukin-6 (IL-6) in IgE/Ag stimulated BMMCs. Analysis of the signaling pathways demonstrated that spinacetin inhibited activation of Syk, linker of activated T cells (LAT), phospholipase Cγ (PLCγ), cytosolic phospholipase A (cPLA), MAPKs, Akt/NF-κB, and intracellular Ca mobilization but with no effect on Fyn and Lyn. On the other hand, spinacetin suppressed IgE/Ag-induced activation of RBL-2H3 cells with inhibition against phosphorylation of extracellular signal regulated-protein kinase (ERK), c-Jun-NH-terminal kinase (JNK), p38 MAPKs, PLCγ, translocation of cPLA, and Akt/IκBα/NF-κB signal. However, spinacetin had no effect on PMA and A23187-induced activation of HMC-1. Furthermore, oral administration of spinacetin dose-dependently attenuated IgE/Ag-mediated PCA reaction in mouse model. Taken together, spinacetin showed the activities in preventing inflammatory processes, which might be at least partially attributed to the abolishment of Syk-dependent activation of IgE/Ag-mediated mast cells.
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http://dx.doi.org/10.3389/fphar.2018.00824DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6077219PMC
July 2018

Analysis of the causes of the misdiagnosis of hereditary spherocytosis.

Oncol Rep 2018 Sep 13;40(3):1451-1458. Epub 2018 Jul 13.

Department of Clinical Laboratory, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, Zhuang Autonomous Region, P.R. China.

Hereditary spherocytosis (HS) is an inherited hemolytic disease with clinical diversities. The aim of the present study was to examine the reasons for prolonged misdiagnosis and mistherapy of HS in a Chinese patient, and to summarize the laboratory screening and treatment methods for this disease in increasing the knowledge towards HS. Clinical data of the proband was reviewed. The proband was first screened by detection of eosin-5'-maleimide (EMA)-labeled red blood cells (RBCs) using flow cytometry. The type of protein defect in the extracted RBC membrane proteins was confirmed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Mutant fragments were verified using direct DNA sequencing and matrix-assisted laser desorption/ionization time of flight (MALDI-TOF) mass spectroscopy. The proband showed a significant hemolytic tendency and significant reduction in the number of EMA-labeled RBCs. DNA sequencing indicated three site mutations in the SPTA1 gene, including His54Pro, Leu1858Val and 6531-12C>T. Additional DNA analysis of the three mutations in the parents of the proband showed that both the Leu1858Val and 6531‑12C>T mutations were carried by the father and the His54Pro mutation was carried by the mother. Moreover, the mutated peptides were identified by MALDI-TOF mass spectroscopy. HS has diverse clinical manifestations and is easily missed, misdiagnosed and mistreated. Therefore, a comprehensive analysis involving a routine blood test, blood smear, EMA labeling (flow cytometry) and SDS-PAGE can effectively distinguish HS from thalassemia, glucose-6-phosphate deficiency, iron-deficiency anemia and autoimmune hemolytic anemia.
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http://dx.doi.org/10.3892/or.2018.6578DOI Listing
September 2018

Clinical features and the molecular biomarkers of olfactory neuroblastoma.

Pathol Res Pract 2018 Aug 10;214(8):1123-1129. Epub 2018 Jun 10.

Tianjin Key Laboratory on Technologies Enabling Development of Clinical Therapeutics and Diagnostics, School of Pharmacy, Tianjin Medical University, Tianjin 300070, China; Research Center of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China. Electronic address:

Olfactory neuroblastoma (ONB) is a kind of rare and complex head and neck tumor. The reports on this field are very scarce due to the low morbidity. Here, we summarized the clinical features and prognosis of ONB through analysis of 10 cases, and determined the phosphorylation status of some molecules known to be involved in carcinogesis such as Akt, Erk, Stat3 and Stat5 in ONB tissue. Ten ONB patients were recruited in this study, 6 male and 4 female, ranging from 26 to 66 years old. In the 10 cases, 6 were diagnosed as late T stage (T/T), 6 were at late Kadish stage (C/D) and 3 were at high Hyams grade (Ⅲ), which indicated a poorer prognosis. Patient characteristics-gender and tumor features were evaluated with respect to the overall survival (OS) through univariate analysis. The result indicated that the OS of male is obviously higher than that of female after a series of combined treatment. The OS of ONB patients in the late stage or high grade is lower than those in early stages or low grade. Moreover, p-Akt, p-Erk, p-Stat3 and p-Stat5 was detected in 5 (50%), 9 (90%), 7 (70%) and 0 patients (0%), respectively, suggesting the former 3 molecules might be potential biomarkers for diagnosis of ONB.
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http://dx.doi.org/10.1016/j.prp.2018.06.002DOI Listing
August 2018