Publications by authors named "Qiaonan Guo"

10 Publications

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Hsa-mir-3163 and CCNB1 may be potential biomarkers and therapeutic targets for androgen receptor positive triple-negative breast cancer.

PLoS One 2021 19;16(11):e0254283. Epub 2021 Nov 19.

Thyroid & Breast Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, China.

Breast cancer (BC) is the most common malignancy in female, but the role of androgen receptor (AR) in triple-negative breast cancer (TNBC) is still unclear. This study aimed to exam the performance of innovative biomarkers for AR positive TNBC in diagnosis and therapies. Four datasets (GSE42568, GSE45827, GSE54002 and GSE76124) were analyzed by bioinformatic methods and the differential expression genes (DEGs) between the AR positive TNBC tissues and normal tissues were firstly identified by limma package and Venn diagrams. Next, Gene Ontologies (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed to explore the relationship between these DEGs. Then, the Protein-protein interaction (PPI) network was constructed. CytoHubba and bioinformatic approaches including Molecular Complex Detection (MCODE), Gene Expression Profiling Interactive Analysis (GEPIA), the Kaplan-Meier (KM) plotter and The Human Pro-tein Atlas (THPA) were used to identify the hub genes. Lastly, a miRNA-hub-gene regulatory axis was constructed by use of Target Scan database and ENCORI database. As a result, a total of 390 common DEGs were identified, including 250 up-regulated and 140 down-regulated. GO and KEGG enrichment analysis showed that the up-regulated DEGs were mostly enriched in the cell division, mitotic nuclear division, nucleosome, midbody, protein heterodimerization activity, cadherin binding involved in cell-cell adhesion, systemic lupus erythematosus and alcoholism, while the down-regulated DEGs were mainly enriched in carbohydrate metabolic process, extracellular space, extracellular region, zinc ion binding and microRNAs in cancer. Then, 13 hub genes (CCNB2, FOXM1, HMMR, MAD2L1, RRM2, TPX2, TYMS, CEP55, AURKA, CCNB1, CDK1, TOP2A, PBK) were selected. The survival analysis revealed that only CCNB1 was associated with significantly poor survival (P <0.05) in TNBC patients. Finally, we found that hsa-miR-3163 took part in the regulation of CCNB1 and constructed a potential hsa-miR-3163-CCNB1 regulatory axis. The results of current study suggest that CCNB1 and hsa-miR-3163 may serve as highly potential prognostic markers and therapeutic targets for AR positive TNBC. Our findings may make contributions to the diagnosis and therapies of AR positive TNBC.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0254283PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8604295PMC
December 2021

Characterization of Exosome-Related Gene Risk Model to Evaluate the Tumor Immune Microenvironment and Predict Prognosis in Triple-Negative Breast Cancer.

Front Immunol 2021 1;12:736030. Epub 2021 Oct 1.

Department of Breast and Thyroid Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, China.

Background: As a kind of small membrane vesicles, exosomes are secreted by most cell types from multivesicular endosomes, including tumor cells. The relationship between exosomes and immune response plays a vital role in the occurrence and development of tumors. Nevertheless, the interaction between exosomes and the microenvironment of tumors remains unclear. Therefore, we set out to study the influence of exosomes on the triple-negative breast cancer (TNBC) microenvironment.

Method: One hundred twenty-one exosome-related genes were downloaded from ExoBCD database, and IVL, CXCL13, and AP2S1 were final selected because of the association with TNBC prognosis. Based on the sum of the expression levels of these three genes, provided by The Cancer Genome Atlas (TCGA), and the regression coefficients, an exosome risk score model was established. With the median risk score value, the patients in the two databases were divided into high- and low-risk groups. R clusterProfiler package was employed to compare the different enrichment ways between the two groups. The ESTIMATE and CIBERSORT methods were employed to analyze ESTIMATE Score and immune cell infiltration. Finally, the correlation between the immune checkpoint-related gene expression levels and exosome-related risk was analyzed. The relationship between selected gene expression and drug sensitivity was also detected.

Results: Different risk groups exhibited distinct result of TNBC prognosis, with a higher survival rate in the low-risk group than in the high-risk group. The two groups were enriched by immune response and biological process pathways. A better overall survival (OS) was demonstrated in patients with high scores of immune and ESTIMATE rather than ones with low scores. Subsequently, we found that CD4-activated memory T cells and M1 macrophages were both upregulated in the low-risk group, whereas M2 macrophages and activated mast cell were downregulated in the low-risk group in patients from the TCGA and GEO databases, respectively. Eventually, four genes previously proposed to be targets of immune checkpoint inhibitors were evaluated, resulting in the expression levels of CD274, CTLA4, LAG3, and TIM3 being higher in the low-risk group than high-risk group.

Conclusion: The results of our study suggest that exosome-related risk model was related to the prognosis and ratio of immune cell infiltration in patients with TNBC. This discovery may make contributions to improve immunotherapy for TNBC.
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http://dx.doi.org/10.3389/fimmu.2021.736030DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8517454PMC
December 2021

Rab7 Is Associated with Poor Prognosis of Gastric Cancer and Promotes Proliferation, Invasion, and Migration of Gastric Cancer Cells.

Med Sci Monit 2020 Jun 27;26:e922217. Epub 2020 Jun 27.

Department of Surgical Oncology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, China (mainland).

BACKGROUND Rab7 belongs to the Ras oncogene family. Many studies have shown that its dysfunction is associated with many types of malignant tumors, but its effect on the pathogenesis of gastric cancer (GC) is still unknown. Therefore, we investigated the effect and mechanism of Rab7 in GC. MATERIAL AND METHODS The expression of Rab7 in GC and adjacent tissues was detected by immunohistochemistry, Western blot analysis, and qRT-PCR. The relationship of Rab7 with clinicopathological parameters and prognosis was analyzed. The expressions of Rab7, PI3K, and AKT in GC cells were assessed by Western blot. Overexpressed and silenced GC cell lines were constructed and AGS cells were treated with LY294002. The proliferation capacity of GC cells was detected by CCK8 assay, cell cycle changes were detected by flow cytometry, and the invasion and migration abilities of GC cells were assessed by transwell assay. RESULTS The expression of Rab7 was upregulated in the samples and cells, and was positively correlated with lymph node metastasis but negatively correlated with histological differentiation and clinical prognosis. In cell function experiments, overexpression of Rab7 induced the transition from S phase to G2 phase and promoted the proliferation, invasion, and migration of GC cells. Our assessment of the molecular mechanism showed that Rab7 promoted the phosphorylation of PI3K and AKT in GC cells. Incubation with the PI3K inhibitor Ly294002 impaired the enhanced effect of Rab7 overexpression on proliferation, migration, and invasion abilities of GC cells. These results show that the Rab7 affects GC cell progression by modulating the PI3K/AKT pathway. CONCLUSIONS Rab7 could be a prognostic biomarker and therapeutic target of the PI3K/AKT pathway in GC.
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http://dx.doi.org/10.12659/MSM.922217DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7339976PMC
June 2020

Pathological evidence for residual SARS-CoV-2 in pulmonary tissues of a ready-for-discharge patient.

Cell Res 2020 06 28;30(6):541-543. Epub 2020 Apr 28.

Institute of Pathology & Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, 400038, China.

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http://dx.doi.org/10.1038/s41422-020-0318-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7186763PMC
June 2020

LncRNA growth arrest-specific transcript 5 targets miR-21 gene and regulates bladder cancer cell proliferation and apoptosis through PTEN.

Cancer Med 2020 04 18;9(8):2846-2858. Epub 2020 Feb 18.

Department of Clinical Laboratory, Huadu District People's Hospital, Southern Medical University, Guangzhou, China.

The aim of this study was to investigate the mechanism by which growth arrest-specific transcript 5 (GAS5) regulates bladder cancer cells. Bladder cancer samples were collected and tested for experiment. Dual-luciferase reporter assay was used to verify the downstream target genes for GAS5 and miR-21. The expression level of GAS5 was decreased and that of miR-21 was increased, indicating a negative correlation between the two. Patients with high GAS5 level and low miR-21 level had relatively longer survival rates. GAS5 inhibited bladder cancer cells proliferation and promoted apoptosis, and miR-21 had the opposite effects. MiR-21 was a direct target for GAS5, whereas phosphatase and tensin homolog (PTEN) was a direct target gene of miR-21. Low expression of miR-21 could reverse the proliferative and antiapoptotic effects caused by GAS5 silencing. High levels of GAS5 and low levels of miR-21 might be associated with a higher survival rate in bladder cancer patients. GAS5 could exert antiproliferative and proapoptotic effects on bladder cancer cells through miR-21 and PTEN.
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http://dx.doi.org/10.1002/cam4.2664DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7163107PMC
April 2020

Chronic Microcystin-LR Exposure Induces Hepatocarcinogenesis via Increased Gankyrin in Vitro and in Vivo.

Cell Physiol Biochem 2018 11;49(4):1420-1430. Epub 2018 Sep 11.

Department of Environmental Hygiene, College of Preventive Medicine, Army Medical University, Third Military Medical University, Chongqing, China.

Background/aims: Our recent study indicated that the serum microcystin-LR (MC-LR) level is positively linked to the risk of human hepatocellular carcinoma (HCC). Gankyrin is over-expressed in cancers and mediates oncogenesis; however, whether MC-LR induces tumor formation and the role of gankyrin in this process is unclear.

Methods: We induced malignant transformation of L02 liver cells via 35 passages with exposure to 1, 10, or 100 nM MC-LR. Wound healing, plate and soft agar colony counts, and nude mice tumor formation were used to evaluate the tumorigenic phenotype of MC-LR-treated cells. Silencing gankyrin was used to confirm its function. We established a 35-week MC-LR exposure rat model by twice weekly intraperitoneal injection with 10 μg/kg body weight. In addition, 96 HCC patients were tested for tumor tissue gankyrin expression and serum MC-LR levels.

Results: Chronic low-dose MC-LR exposure increased proliferation, mobility, clone and tumor formation abilities of L02 cells as a result of gankyrin activation, while silencing gankyrin inhibited the carcinogenic phenotype of MC-LR-treated cells. MC-LR also induced neoplastic liver lesions in Sprague-Dawley rats due to up-regulated gankyrin. Furthermore, a trend of increased gankyrin was observed in humans exposed to MC-LR.

Conclusion: These results suggest that MC-LR induces hepatocarcinogenesis in vitro and in vivo by increasing gankyrin levels, providing new insight into MC-LR carcinogenicity studies.
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http://dx.doi.org/10.1159/000493446DOI Listing
October 2018

Clinical characteristics of primary intestinal NK/T cell lymphoma, nasal type: Case series and review of the literature.

Pathol Res Pract 2018 Aug 25;214(8):1081-1086. Epub 2018 May 25.

Department of Gastroenterology, Xinqiao Hospital of Third Military Medicine University, Chongqing, 400037, China. Electronic address:

Background: Primary intestinal NK/T cell lymphoma is rare but aggressive and exhibits a poor prognosis. Little is known about its clinical characteristics because few studies with small sample sizes have been reported.

Aims: To provide clinicopathological features and endoscopic findings and to summarize the treatment outcomes of primary intestinal NK/T cell lymphoma to improve our understanding of this disease.

Methods: Between January 2011 to December 2016, 13 patients with confirmed primary gastrointestinal NK/T cell lymphoma at our center were described, and an updated literature review was provided.

Results: In this series of 13 cases, 69.23% were men, the median age was 39 years, and the median survival was 6 months. The common clinical manifestations included abdominal pain (76.92%) and gastrointestinal bleeding (46.15%). Lymphomas were common in the large intestine (69.23%). In 76.92% of patients, the clinical staging was stage I, and all 13 patients manifested ulcerative lesions and no tumor mass on endoscopy. The clinical characteristics of primary intestinal NK/T cell lymphomas were similar to results in existing literature.

Conclusion: Intestinal NK/T cell lymphoma shows nonspecific clinical features and poor prognosis, which is mainly expressed as ulcers on endoscopy. Emergency surgery may be an adverse prognostic factor of lymphoma, since it is prone to progress toward gastrointestinal perforation.
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http://dx.doi.org/10.1016/j.prp.2018.05.013DOI Listing
August 2018

Formyl peptide receptors promotes neural differentiation in mouse neural stem cells by ROS generation and regulation of PI3K-AKT signaling.

Sci Rep 2017 03 16;7(1):206. Epub 2017 Mar 16.

Department of Spine Surgery, Daping Hospital, Third Military Medical University, Chongqing, 400042, China.

This study aimed to determine whether formyl peptide receptors (FPRs) regulated the differentiation of neural stem cells (NSCs). FPRs promote the migration of NSCs both in vitro and in vivo. However, the role of FPRs during differentiation of NSCs is unknown. Analysis by Western blot showed significantly increased expression of FPR1 and FPR2 during differentiation of NSCs. The activation of FPRs promotes NSCs to differentiate into neurons with more primary neurites and branch points and longer neurites per cell. Meanwhile, this activation also inhibits the differentiation of NSC into astrocytes. This bidirectional effect can be inhibited by the FPRs-specific inhibitor. Moreover, it was found that the activation of FPRs increased the generation of reactive oxygen species (ROS) and phosphorylation of AKT in the NSCs, while N-acetylcysteine and LY294002 inhibited the FPRs-stimulated increase in ROS generation and AKT phosphorylation, and blocked the FPRs-stimulated neural differentiation into neurons. Therefore, FPRs-stimulated neural differentiation was mediated via ROS and PI3K-AKT signaling pathways. Collectively, the present findings provided a novel insight into the functional role of FPRs in neurogenesis, with important implications for its potential use as a candidate for treating brain or spinal cord injury.
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http://dx.doi.org/10.1038/s41598-017-00314-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5428260PMC
March 2017

Formylpeptide Receptors Promote the Migration and Differentiation of Rat Neural Stem Cells.

Sci Rep 2016 05 13;6:25946. Epub 2016 May 13.

Department of Spine Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042, China.

Neural stem cells (NSCs) bear characteristics for proliferation, migration and differentiation into three main neural cell type(s): neurons, astrocytes and/or oligodendrocytes. Formylpeptide receptors (Fprs), belonging to the family of G protein-coupled chemoattractant receptors, have been detected on neurons in the central nervous system (CNS). Here, we report that Fpr1 and Fpr2 are expressed on NSCs as detected with immunohistochemistry, RT-PCR and WB assays. In addition, Fpr1 and Fpr2 promoted NSC migration through F-actin polymerization and skewed NSC differentiation to neurons. Our study demonstrates a unique role of Fpr1 and Fpr2 in NSCs and opens a novel window for cell replacement therapies for brain and spinal cord injury.
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http://dx.doi.org/10.1038/srep25946DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4865803PMC
May 2016

Intraparenchymal schwannoma of the medulla oblongata. Case report.

J Neurosurg 2003 Mar;98(3):621-4

Department of Neurosurgery, Southwest Hospital, Third Military Medical University, Shapingba District, Chongqing, People's Republic of China.

A 48-year-old man presented with a rare intraparenchymal schwannoma of the medulla oblongata. After he underwent gamma knife surgery, the patient's condition deteriorated and the mass, which at the time was thought to be a glioma, became larger on magnetic resonance images. The mass was resected through a suboccipital craniectomy via the transcerebellomedullary fissure approach. The tumor, which was moderately firm but distinct from the surrounding parenchyma, was removed totally. Postoperative histological and immunohistochemical examinations confirmed the diagnosis of a benign schwannoma. Brainstem schwannomas can be cured by microneurosurgery. It is important to distinguish these tumors from glioma. The main theories on the cause(s) of this lesion are briefly reviewed.
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http://dx.doi.org/10.3171/jns.2003.98.3.0621DOI Listing
March 2003
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