Publications by authors named "Chaoyang Zhu"

24 Publications

  • Page 1 of 1

Regulation of maltocin synthesis in Stenotrophomonas maltophilia by positive and negative regulators.

Res Microbiol 2022 Jul-Sep;173(6-7):103956. Epub 2022 May 13.

College of Life Sciences, Wuhan University, Wuhan 430072, China. Electronic address:

Maltocin P28, produced by Stenotrophomonas maltophilia P28, is an R-type phage tail-like bacteriocin (PTLB). Its gene cluster consists of 23 putative genes, including nine nonstructural genes and fourteen structural genes. In this work, three nonstructural genes, mpsA, mpsH and mpsR, were found to encode transcriptional regulators to control maltocin P28 synthesis. MpsA activated the transcription of mpsH and lysis genes. MpsH activated the transcription of structural genes. Under normal growth conditions, MpsR repressed the transcription of mpsA and the structural genes, as well as its own. When S. maltophilia P28 was treated with mitomycin C, an immediate and significant decrease in the amount of MpsR was observed, followed by derepressed expression of mpsA, mpsR and structural genes, a marked rise in the expression of all regulatory and structural genes, and finally a clear increase in the maltocin P28 production. Neither the recA gene nor the lexA gene was found to be involved in the induced synthesis of maltocin P28. Our study indicated that a unique mechanism regulates the expression of maltocin genes in S. maltophilia, representing a novel strategy for balancing the expression of PTLB genes in bacteria.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.resmic.2022.103956DOI Listing
July 2022

Ningmitai capsule promotes calculi expulsion after RIRS for 10-20-mm upper urinary stones: a multicenter, prospective, randomized controlled trial.

Urolithiasis 2022 Apr 25;50(2):205-214. Epub 2022 Jan 25.

Department of Urology, The Second Affiliated Hospital of Zhengzhou University, No. 2 Jingba Road, Zhengzhou, 450014, Henan, China.

To evaluate the efficacy and safety of the use of Ningmitai capsule as an adjunctive stone expulsion therapy after RIRS. All patients were diagnosed with upper urinary tract calculi measuring 10-20 mm. The patients who successfully underwent RIRS were randomly assigned to the NMT capsule group (Ningmitai capsule, 1.52 g, three times daily) or the control group for 4 weeks based on the random number table method. The primary endpoints were the stone expulsion rate (SER) and stone-free rate (SFR). The average stone expulsion time (SET), average stone-free time (SFT) and complications were recorded. Between July 2, 2019, and December 17, 2020, 220 participants successfully underwent RIRS across 6 centers; 123 of them were randomized according to the exclusion criteria, and 102 (83%) were included in the primary analysis. The SERs on the 3rd, 7th, 14th and 28th days were significantly increased in the NMT capsule group compared with the control group (78.95% vs. 31.11%, 92.98% vs. 55.56%, 94.74% vs. 64.44%, 100% vs. 82.22%, respectively, p < 0.05). The SFRs on the 3rd and 7th days were not different (p > 0.05), while those on the 14th and 28th days were higher in the NMT capsule group (63.16% vs. 24.44% and 92.98% vs. 68.89%, p < 0.05). The average SET and average SFT of the NMT capsule group were remarkably shorter than those of the control group (p < 0.001). During the follow-up period, there were no significant differences in urine RBC counts between the two groups (p > 0.05). The urine WBC counts of the NMT capsule group were significantly lower than those of the control group on the 14 day (p = 0.011), but there was no difference on the 3rd, 7th or 28th day (p > 0.05). The analgesic aggregate of the NMT capsule group was also much lower (p = 0.037). There were no significant differences in adverse events (p > 0.05), and they improved significantly without sequelae. This study indicated that NMT capsules can significantly promote stone clearance and are more effective and safer for upper urinary calculi after RIRS.Trial registration Chinese Clinical Trial Registration No. ChiCTR1900024151.Date of registration June 28, 2019.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00240-021-01296-wDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8786453PMC
April 2022

Research on the evolution and driving forces of the manufacturing industry during the "13th five-year plan" period in Jiangsu province of China based on natural language processing.

PLoS One 2021 18;16(8):e0256162. Epub 2021 Aug 18.

Institute of Industrial Economics of CASS, Beijing, China.

The development of China's manufacturing industry has received global attention. However, research on the distribution pattern, changes, and driving forces of the manufacturing industry has been limited by the accessibility of data. This study proposes a method for classifying based on natural language processing. A case study was conducted employing this method, hotspot detection and driving force analysis, wherein the driving forces industrial development during the "13th Five-Year plan" period in Jiangsu province were determined. The main conclusions of the empirical case study are as follows. 1) Through the acquisition of Amap's point-of-interest (POI, a special point location that commonly used in modern automotive navigation systems.) data, an industry type classification algorithm based on the natural language processing of POI names is proposed, with Jiangsu Province serving as an example. The empirical test shows that the accuracy was 95%, and the kappa coefficient was 0.872. 2) The seven types of manufacturing industries including the pulp and paper (PP) industry, metallurgical chemical (MC) industry, pharmaceutical manufacturing (PM) industry, machinery and electronics (ME) industry, wood furniture (WF) industry, textile clothing (TC) industry, and agricultural and food product processing (AF) industry are drawn through a 1 km× 1km projection grid. The evolution map of the spatial pattern and the density field hotspots are also drawn. 3) After analyzing the driving forces of the changes in the number of manufacturing industries mentioned above, we found that manufacturing base, distance from town, population, GDP per capita, distance from the railway station were the significant driving factors of changes in the manufacturing industries mentioned above. The results of this research can help guide the development of manufacturing industries, maximize the advantages of regional factors and conditions, and provide insight into how the spatial layout of the manufacturing industry could be optimized.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0256162PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8372942PMC
December 2021

TaWRKY10 plays a key role in the upstream of circadian gene TaLHY in wheat.

Plant Sci 2021 Sep 11;310:110973. Epub 2021 Jun 11.

College of Life Sciences, Sichuan Agricultural University, Ya'an, 625014, PR China. Electronic address:

TaLHY is an MYB transcription factor (TF) that is upregulated by salicylic acid induction and shows circadian rhythms. However, the study of the upstream regulatory factors is still unclear. In this study, we cloned the promoter sequence of the TaLHY homologous genes, verified the activity of the promoters, and identified important regions that affect promoter activity. Furthermore, we explored a possible upstream regulator of TaLHY, named TaWRKY10, which played a key role in the expression of TaLHY. We found that the three promoters pTaLHYa, pTaLHYb, and pTaLHYd had transcriptional activity in wheat protoplasts. All three promoters have W-Box, which can bind to WRKY TFs. Using virus-induced gene silencing (VIGS), after silencing TaWRKY10, the resistance of ChuanNong 19 (CN19) to stripe rust pathogen strain CYR32 was lost, and the expression level of the TaLHY homologous gene decreased. At the same time, in wheat protoplasts, the transcriptional activity of TaLHY homologous promoters improved after TaWRKY10 overexpression. This indicates that TaWRKY10 is a key gene for wheat immune response to stripe rust, and this gene may bind to TaLHYa, TaLHYb, and TaLHYd promoters to regulate the expression of TaLHY.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.plantsci.2021.110973DOI Listing
September 2021

Effectors of f. sp. Suppressing the Pathogenic-Associated Molecular Pattern-Triggered Immune Response Were Screened by Transient Expression of Wheat Protoplasts.

Int J Mol Sci 2021 May 7;22(9). Epub 2021 May 7.

College of Life Science, Sichuan Agricultural University, Ya'an 625014, China.

f. sp. () is an important pathogen of wheat ( L.) stripe rust, and the effector protein secreted by haustoria is a very important component involved in the pathogenic process. Although the candidate effector proteins secreted by haustoria have been predicted to be abundant, few have been functionally validated. Our study confirmed that chitin and flg22 could be used as elicitors of the pathogenic-associated molecular pattern-triggered immune (PTI) reaction in wheat leaves and that could be used as a marker gene to detect the PTI reaction. In addition, the experimental results were consistent in wheat protoplasts. A rapid and efficient method for screening and identifying the effector proteins of was established by using the wheat protoplast transient expression system. Thirty-nine haustorial effector genes were successfully cloned and screened for expression in the protoplast. We identified three haustorial effector proteins, PSEC2, PSEC17, and PSEC45, that may inhibit the response of wheat to PTI. These proteins are localized in the somatic cytoplasm and nucleus of wheat protoplasts and are highly expressed during the infection and parasitism of wheat.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/ijms22094985DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8125866PMC
May 2021

Circular RNA_0001495 increases Robo1 expression by sponging microRNA-527 to promote the proliferation, migration and invasion of bladder cancer cells.

Carcinogenesis 2021 08;42(8):1046-1055

Department of Urology Surgery, Huaihe Hospital of Henan University, Kaifeng 475000, P.R. China.

Bladder cancer (BCa) is a heterogeneous disease that poses great threats on public health. Increasing studies have identified the vital functions of circular RNAs (circRNAs) in BCa treatment. Hence, this current study set out to explore the modulatory role of circ_0001495 in BCa development. First, the expression of circ_0001495 was determined by reverse transcription quantitative polymerase chain reaction. Cell biological processes were then analyzed after altering the circ_0001495 expression in T24 cells. Next, interactions among circ_0001495, microRNA-527 (miR-527) and roundabout guidance receptor 1 (Robo1) were investigated by dual luciferase reporter gene assay, RNA pull down assay and FISH assay. Lastly, xenograft tumors in nude mice were established to explore the effect of circ_0001495 in vivo. It was found that circ_0001495 was highly expressed in BCa tissues and cells, and was further correlated with poor prognosis in BCa patients. In addition, circ_0001495 inhibited the activity of miR-527 by acting as a sponge to sponge miR-527, which further elevated the Robo1 expression. Lastly, circ_0001495 was found to promote the proliferation, migration and invasion of BCa cells in vitro through the miR-527/Robo1 axis and promote the growth and metastasis of BCa tumors in vivo. Altogether, findings in our study highlight the promoting role of circ_0001495 in the progression of BCa by increasing Robo1 via sponging miR-527, representing a promising target for BCa management.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1093/carcin/bgab040DOI Listing
August 2021

Habitual consumption of alcohol with meals and lung cancer: a Mendelian randomization study.

Ann Transl Med 2021 Feb;9(3):263

Sun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.

Background: The objective of this study was to determine the causal relationship between habitual alcohol consumption with meals and lung cancer.

Methods: Public genetic summary data from two large consortia [the Neale Lab and the International Lung Cancer Consortium (ILCCO)] were used for analysis. As the instrumental variables of habitual alcohol consumption with meals, data on genetic variants were retrieved from Neale Lab. Additionally, genetic data from other consortia [Global Lipid Genetics Consortium (GLGC), Tobacco, Alcohol and Genetics (TAG), Genetic Investigation of Anthropocentric Traits (GIANT)] were utilized to determine whether alcohol could causally alter some general risk factors for lung cancer. The primary outcome was the risk of lung cancer (11,348 cases and 15,861 controls in the ILCCO). The R package TwoSampleMR was used for analysis.

Results: Based on the inverse variance weighted method, the results of the two-sample Mendelian randomization (MR) analyses indicated that commonly consuming alcohol with meals was a protective factor, reducing lung cancer risk [odds ratio (OR) 0.175, 95% confidence interval (CI): 0.045-0.682, P=0.012]. The heterogeneity analysis revealed that the causal relationship analyses of different types of lung cancer all had low heterogeneity (P>0.05). The horizontal pleiotropic study showed that major bias was unlikely. The MR assumptions did not seem to be violated. The causal relationship analyses between habitual alcohol consumption with meals and some risk factors for cancers showed that this alcohol consumption habit was a beneficial factor for reducing body mass index (BMI) and the number of cigarettes smoked per day.

Conclusions: Habitual appropriate alcohol consumption with meals is a protective factor for the development of lung cancer.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.21037/atm-20-3063DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7940946PMC
February 2021

Long Non-coding RNA Inhibits VEGFA Expression via Enhancing Its DNA Methylation Leading to Tumor Suppression in Renal Carcinoma.

Front Oncol 2020 2;10:1082. Epub 2020 Sep 2.

Department of Urinary Surgery, Huaihe Hospital, Henan University, Kaifeng, China.

Long non-coding RNA (lncRNA ) plays a critical role in numerous malignancies. However, the function of lncRNA in renal carcinoma (RC) remains enigmatic. The purpose of this study is to characterize the effects of lncRNA on RC progression. The expression pattern of lncRNA and the vascular endothelial growth factor A (VEGFA) in RC tissues and cells was characterized by RT-qPCR and Western blot analysis. The roles of lncRNA and VEGFA in the progression of RC were studied by gain- or loss-of-function experiments. Bioinformatics data analysis was used to predict CpG islands in the promoter region. MSP was applied to detect the level of DNA methylation in RC cells. The interaction between lncRNA and VEGFA was identified by RNA immunoprecipitation and RNA-protein pull down assays. Recruitment of DNA methyltransferases (Dnmt) to the promoter region was achieved by chromatin immunoprecipitation. The subcellular localization of lncRNA was detected by fractionation of nuclear and cytoplasmic RNA. Cell viability was investigated by CCK-8 assay, cell migration was tested by transwell migration assay, and apoptosis was analyzed by flow cytometry. The expression of epithelial-mesenchymal transition-related and apoptotic factors was evaluated by Western blot analysis. Finally, the effect of the lncRNA /VEGFA axis was confirmed in an tumor xenograft model. LncRNA was poorly expressed in RC tissues and cells with a primary localization in the nucleus, while VEGFA was highly expressed. Overexpression of lncRNA or knockdown of inhibited cell proliferation and migration and induced the apoptosis of RC cells. Bioinformatics analysis indicated the presence of CpG islands in the promoter region. Lack of methylation at specific sites in the promoter region was detected through MSP assay. We found that lncRNA was able to inhibit VEGFA expression through recruitment of Dnmt1, Dnmt3a, and Dnmt3b to the promoter region. LncRNA was also able to suppress RC tumor growth repression of VEGFA in an mouse xenograft model. Our data shows that by downregulating expression in RC, the lncRNA has tumor-suppressive potential.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fonc.2020.01082DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7492562PMC
September 2020

LncRNA EMX2OS, Regulated by TCF12, Interacts with FUS to Regulate the Proliferation, Migration and Invasion of Prostate Cancer Cells Through the cGMP-PKG Signaling Pathway.

Onco Targets Ther 2020 21;13:7045-7056. Epub 2020 Jul 21.

Department of Urinary Surgery, Huaihe Hospital of Henan University, Kaifeng 475000, People's Republic of China.

Background: LncRNA EMX2OS (EMX2 opposite strand/antisense RNA) is notably downregulated in prostate cancer (PCa) tissues and may be regarded as a potential molecular biomarker for diagnosis and prognosis. However, its exact role in regulating the development of PCa is obscure.

Methods: The EMX2OS expression was assessed in PCa tissues, paracancer tissues, PCa cells and normal prostate epithelial cells by qPCR. Gain- and loss-of-function experiments were performed to investigate the role of EMX2OS and FUS in cGMP-PKG (cyclic guanosine monophosphate-dependent protein kinase)-mediated proliferation, invasion, and migration in human PCa cell lines DU145 and PC3. Then, the interaction of transcription factor 12 (TCF12) with EMX2OS promoter was confirmed by using the dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assays. RNA binding protein immunoprecipitation and RNA pull-down assays were used to verify the interaction between EMX2OS and FUS protein. Finally, the role of EMX2OS and FUS in tumor growth in vivo was validated in a xenograft nude mouse model.

Results: TCF12 and EMX2OS were both downregulated in PCa tissues and cells, and they negatively regulated cell proliferation, migration and invasion, and activated cGMP-PKG pathway in DU145 and PC3 cells. TCF12 was a transcription factor of EMX2OS. TCF12 and EMX2OS overexpression both down-regulated cell proliferation, migration and invasion, and activated cGMP-PKG pathway in DU145 and PC3 cells. Furthermore, EMX2OS directly bound with FUS protein and had a synergy effect with FUS protein on cGMP-PKG-mediated cell functions, which could be suppressed by (D)-DT-2 (a cGMP-PKG inhibitor). In addition, the overexpression of FUS or EMX2OS individually markedly decreased the volume and weight of tumors in vivo, and co-overexpression of them further inhibited tumor growth.

Conclusion: EMX2OS, transcriptionally regulated by TCF12, played a synergy role with FUS protein in regulating the proliferation, migration and invasion of PCa cells by activating the cGMP-PKG pathway.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.2147/OTT.S243552DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7398891PMC
July 2020

Knockdown of lncRNA PVT1 inhibits prostate cancer progression in vitro and in vivo by the suppression of KIF23 through stimulating miR-15a-5p.

Cancer Cell Int 2020 2;20:283. Epub 2020 Jul 2.

Department of Urology Surgery, The Huaihe Hospital of Henan University, Kaifeng, Henan China.

Background: Prostate cancer (PCa) greatly threatens men's lives, with high incidence and mortality. Recently, the research of long non-coding RNAs (lncRNAs) has made breakthroughs in the development of human cancers. This study aimed to figure out the role and action mechanism of lncRNA PVT1 (PVT1) in PCa.

Methods: The expression of PVT1, microRNA-15a-5p (miR-15a-5p) and kinesin family member 23 (KIF23) was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, apoptosis, migration and invasion were assessed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2--tetrazolium bromide (MTT), flow cytometry and transwell assays, respectively. The protein levels of KIF23 and proliferation, apoptosis, and epithelial-mesenchymal transition (EMT)-related markers were quantified by western blot. The relationship between miR-15a-5p and PVT1 or KIF23 was predicted by starBase v2.0 and verified by dual-luciferase reporter assay. Xenograft assay was conducted to determine the role of PVT1 in vivo.

Results: The expression of PVT1 and KIF23 was enhanced, while miR-15a-5p expression was reduced in PCa tissues and cells. PVT1 interference inhibited proliferation, migration and invasion but promoted apoptosis of PCa cells. MiR-15a-5p was a target of PVT1, and KIF23 was a target of miR-15a-5p. The inhibition of miR-15a-5p reversed the effects of PVT1 interference and suppressed the roles of KIF23 knockdown. KIF23 expression was regulated by PVT1 through miR-15a-5p. PVT1 interference blocked PCa progression in vivo.

Conclusion: PVT1 knockdown had effects on the progression of PCa by inhibiting the expression of KIF23 via enriching miR-15a-5p in vitro and in vivo, suggesting that PVT1 might be a novel biomarker for the treatment of PCa.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s12935-020-01363-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7330980PMC
July 2020

The role of the gene family in ovarian cancer.

Ann Transl Med 2020 Mar;8(5):190

Department of Intensive Care Unit, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China.

Background: Ovarian cancer is a frequently-occurring reproductive system malignancy in females, which leads to an annual of over 100 thousand deaths worldwide.

Methods: The electronic databases, including GEPIA, ONCOMINE, Metascape, and Kaplan-Meier Plotter, were used to examine both survival and transcriptional data regarding the cell division cycle associated () gene family among ovarian cancer patients.

Results: All genes expression levels were up-regulated in ovarian cancer tissues relative to those in non-carcinoma ovarian counterparts. Besides, expression levels were related to the late tumor stage. In addition, the Kaplan-Meier Plotter database was employed to carry out survival analysis, which suggested that ovarian cancer patients with increased expression levels had poor overall survival (OS) (P<0.05). Moreover, ovarian cancer patients that had up-regulated mRNA expression levels of had markedly reduced progression-free survival (PFS) (P<0.05); and up-regulated expression showed remarkable association with reduced post-progression survival (PPS) (P<0.05). Additionally, the following processes were affected by genes alterations, including R-HAS-2500257: resolution of sister chromatid cohesion; GO:0051301: cell division; CORUM: 1118: Chromosomal passenger complex (CPC, including , , and ); CORUM: 127: NDC80 kinetochore complex; M129: PID PLK1 pathway; and GO: 0007080: mitotic metaphase plate congression, all of which were subjected to marked regulation since the alterations affected genes.

Conclusions: Up-regulated gene expression in ovarian cancer tissues probably played a crucial part in the occurrence of ovarian cancer. The up-regulated expression levels were used as the potential prognostic markers to improve the poor ovarian cancer survival and prognostic accuracy. Moreover, genes probably exerted their functions in tumorigenesis through the PLK1 pathway.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.21037/atm.2020.01.99DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7154490PMC
March 2020

Epitope-directed antibody selection by site-specific photocrosslinking.

Sci Adv 2020 04 1;6(14):eaaz7825. Epub 2020 Apr 1.

Key Laboratory of Protein and Peptide Pharmaceuticals, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.

Currently, there are no methods available offering solutions to select and identify antibodies binding to a specific conformational epitope of an antigen. Here, we developed a method to allow epitope-directed antibody selection from a phage display library by photocrosslinking bound antibodies to a site that specifically incorporates a noncanonical amino acid, -benzoyl-l-phenylalanine (pBpa), on the target antigen epitope. By one or two rounds of panning against antibody phage display libraries, those hits that covalently bind to the proximity site of pBpa on specific epitopes of target antigens after ultraviolet irradiation are enriched and selected. This method was applied to specific epitopes on human interleukin-1β and complement 5a. In both cases, more than one-third of hits identified bind to the target epitopes, demonstrating the feasibility and versatility of this method.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1126/sciadv.aaz7825DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7112767PMC
April 2020

miR-204 Negatively Regulates Cell Growth And Metastasis By Targeting ROBO4 In Human Bladder Cancer.

Onco Targets Ther 2019 16;12:8515-8524. Epub 2019 Oct 16.

Department of Urology, Henan University Huaihe Hospital, Kaifeng 475000, People's Republic of China.

Background: MicroRNAs (miRNAs) are well characterized for their important roles in human cancers by influencing various aspects of malignancy. Till now, the function and mechanism of miR-204, a tumor suppressor in several cancers, remain unclear in bladder cancer (BC). Here, we intend to explore its roles in BC progression.

Methods: qRT-PCR was applied to determine miR-204 and ROBO4 expression in BC tissues and cell lines. miR-204 expression with clinicopathological features was analyzed. The impacts of miR-204 on BC cell growth and metastasis in vitro were evaluated by both loss-of-function and gain-of-function assays (CCK-8, crystal violet staining, wound healing and transwell assays). Furthermore, qRT-PCR, Western blot and luciferase reporter assays were used to validate the targeting of ROBO4 by miR-204. Finally, linear regression was performed to analyze the correlation of miR-204 and ROBO4 in BC tissues.

Results: Expression of miR-204 was markedly decreased in BC tissues and cell lines were compared with respective controls. Low miR-204 expression was associated with positive advanced T stage and lymph node metastasis. Cellular function studies revealed that miR-204 inhibited BC cell growth, migration and invasion. Mechanistic exploration found that miR-204 directly targeted ROBO4. Rescue assays indicated that ROBO4 restoration could reverse the antitumor effects of miR-204 in BC. Finally, ROBO4 was significantly correlated with miR-204 levels inversely.

Conclusion: miR-204 might serve as a tumor suppressor in BC by targeting ROBO4.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.2147/OTT.S205023DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6801631PMC
October 2019

Spatial Pyramid-Enhanced NetVLAD With Weighted Triplet Loss for Place Recognition.

IEEE Trans Neural Netw Learn Syst 2020 Feb 26;31(2):661-674. Epub 2019 Apr 26.

We propose an end-to-end place recognition model based on a novel deep neural network. First, we propose to exploit the spatial pyramid structure of the images to enhance the vector of locally aggregated descriptors (VLAD) such that the enhanced VLAD features can reflect the structural information of the images. To encode this feature extraction into the deep learning method, we build a spatial pyramid-enhanced VLAD (SPE-VLAD) layer. Next, we impose weight constraints on the terms of the traditional triplet loss (T-loss) function such that the weighted T-loss (WT-loss) function avoids the suboptimal convergence of the learning process. The loss function can work well under weakly supervised scenarios in that it determines the semantically positive and negative samples of each query through not only the GPS tags but also the Euclidean distance between the image representations. The SPE-VLAD layer and the WT-loss layer are integrated with the VGG-16 network or ResNet-18 network to form a novel end-to-end deep neural network that can be easily trained via the standard backpropagation method. We conduct experiments on three benchmark data sets, and the results demonstrate that the proposed model defeats the state-of-the-art deep learning approaches applied to place recognition.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1109/TNNLS.2019.2908982DOI Listing
February 2020

UCA1 promotes cell proliferation and invasion and inhibits apoptosis through regulation of the miR129-SOX4 pathway in renal cell carcinoma.

Onco Targets Ther 2018 1;11:2475-2487. Epub 2018 May 1.

Department of Urology, Huaihe Hospital of Henan University, Kaifeng, Henan.

Background: Renal cell carcinoma (RCC) is the most common cancer in kidney malignancies. UCA1 has been identified as an oncogenic lncRNA in multiple cancers, including RCC. However, the underlying molecular mechanism of UCA1 involved in RCC progression is far from being addressed.

Methods: Reverse-transcription quantitative polymerase chain reaction (RT-qPCR) assays were used to measure expressions of UCA1, miR129, and SOX4 mRNA. Western blot assays were employed to detect SOX4 protein expression. Cell proliferation, invasion, and apoptosis were assessed by CCK-8, Matrigel invasion, and annexin-fluorescein isothiocyanate (FITC) apoptosis-detection assays, respectively. The interaction between UCA1 and miR129 was demonstrated by luciferase, RNA pull-down, and RNA-immunoprecipitation (RIP) assays. Luciferase assays were also used to explore whether UCA1 was able to act as a molecular sponge of miR129 to affect the interplay of miR129 and SOX4.

Results: UCA1 expression was upregulated in RCC tissue and cells, and higher UCA1 expression was associated with advanced pathogenic status and poor prognosis of RCC patients. UCA1 knockdown suppressed proliferation and invasion and induced apoptosis in RCC cells. UCA1 inhibited miR129 expression by direct interaction in RCC cells. miR129 overexpression inhibited cell proliferation and invasion and promoted apoptosis. Moreover, miR129 downregulation abrogated UCA1 knockdown-mediated antiproliferation, anti-invasion, and proapoptosis effects in RCC cells. Furthermore, UCA1 acted as a ceRNA of miR129 to enhance target-gene expression in RCC cells.

Conclusion: UCA1 promoted cell proliferation and invasion and inhibited apoptosis by regulating SOX4 via miR129 in RCC, offering a promising therapeutic target and prognosis marker for RCC patients.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.2147/OTT.S160192DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5937506PMC
May 2018

miR-27b and miR-34a enhance docetaxel sensitivity of prostate cancer cells through inhibiting epithelial-to-mesenchymal transition by targeting ZEB1.

Biomed Pharmacother 2018 Jan 6;97:736-744. Epub 2017 Nov 6.

Department of Urology, Huaihe Hospital of Henan University, Kaifeng, 475000, China.

Docetaxel resistance is a primary clinical obstacle in the therapy of advanced prostate cancer (PCa). Aberrant expression of miR-27b and miR-34a has been revealed to be implicated in drug resistance of different tumors. Nevertheless, the roles of miR-27b and miR-34a in docetaxel resistance of PCa and their molecular mechanisms are far from being elucidated. In this study, we found that miR-27b and miR-34a were significantly downregulated in docetaxel-resistant PCa cells. Gain-of-function experiments showed that overexpression of miR-27b or miR-34a enhanced docetaxel sensitivity and inhibited EMT in docetaxel-resistant PCa cells. Moreover, miR-27b and miR-34a was demonstrated to directly target ZEB1 and suppress ZEB1 expression. Loss-of-function analysis disclosed that ZEB1 knockdown enhanced docetaxel sensitivity and suppressed EMT in docetaxel-resistant PCa cells. Rescue experiments presented that ZEB1 overexpression abolished the effects of miR-27b or miR-34a overexpression on docetaxel sensitivity and EMT in docetaxel-resistant PCa cells. Finally, Tumor xenograft assay confirmed the contribution of miR-27b and miR-34a in improving docetaxel sensitivity in PCa in vivo. In summary, miR-27b and miR-34a overexpression enhanced docetaxel sensitivity of PCa partly through inhibiting EMT by targeting ZEB1, providing new insights into the molecular mechanism of miR-27b and miR-34a in modulating docetaxel resistance and potential therapy targets in advanced PCa.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.biopha.2017.10.163DOI Listing
January 2018

Downregulation of long noncoding RNA TUG1 inhibits proliferation and induces apoptosis through the TUG1/miR-142/ZEB2 axis in bladder cancer cells.

Onco Targets Ther 2017 5;10:2461-2471. Epub 2017 May 5.

Department of Urology Surgery, Huaihe Hospital of Henan University, Kaifeng, People's Republic of China.

Background: Bladder cancer is a common serious disease around the world. Long noncoding RNAs (lncRNAs) have been demonstrated to participate in the development and progression of various cancers, including bladder cancer. The aim of this study was to investigate the effects of lncRNA taurine upregulated gene 1 (TUG1) on proliferation and apoptosis in bladder cancer cell lines and the underlying mechanism.

Methods: The levels of TUG1 were detected by quantitative real time polymerase chain reaction (qRT-PCR) in bladder cancer tissues and cells. The mRNA and protein levels of zinc finger E-box binding homeobox 2 (ZEB2) were measured by qRT-PCR and Western blot analysis, respectively. The functional targets of TUG1 were predicted by online softwares and confirmed by luciferase reporter assay. The effects of TUG1 on cell proliferation and apoptosis were examined by MTT and apoptosis assay, respectively. The expression levels of β-catenin, cyclinD1, and c-Myc in T24 cells were determined by Western blot analysis.

Results: The levels of TUG1 and ZEB2 were significantly increased in bladder cancer tissues and cells. Knockdown of either TUG1 or ZEB2 inhibited proliferation and induced apoptosis in bladder cancer cells. Interestingly, ZEB2 overexpression reversed the effects of TUG1 knockdown on cell proliferation and apoptosis. Moreover, ZEB2 was verified as a direct target of miR-142 and miR-142 could specially bind to TUG1. In addition, downregulation of TUG1 inhibited the Wnt/β-catenin pathway by regulating ZEB2 expression in bladder cancer cells.

Conclusion: Downregulation of TUG1 expression inhibited proliferation and induced apoptosis in bladder cancer cells by targeting ZEB2 mediated by miR-142 through the inactivation of Wnt/β-catenin pathway.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.2147/OTT.S124595DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5426477PMC
May 2017

Association between Spouse/Child Separation and Migration-Related Stress among a Random Sample of Rural-to-Urban Migrants in Wuhan, China.

PLoS One 2016 28;11(4):e0154252. Epub 2016 Apr 28.

Wuhan Centers for Disease Prevention and Control, Wuhan, China.

Background: Millions of people move from rural areas to urban areas in China to pursue new opportunities while leaving their spouses and children at rural homes. Little is known about the impact of migration-related separation on mental health of these rural migrants in urban China.

Methods: Survey data from a random sample of rural-to-urban migrants (n = 1113, aged 18-45) from Wuhan were analyzed. The Domestic Migration Stress Questionnaire (DMSQ), an instrument with four subconstructs, was used to measure migration-related stress. The relationship between spouse/child separation and stress was assessed using survey estimation methods to account for the multi-level sampling design.

Results: 16.46% of couples were separated from their spouses (spouse-separation only), 25.81% of parents were separated from their children (child separation only). Among the participants who married and had children, 5.97% were separated from both their spouses and children (double separation). Spouse-separation only and double separation did not scored significantly higher on DMSQ than those with no separation. Compared to parents without child separation, parents with child separation scored significantly higher on DMSQ (mean score = 2.88, 95% CI: [2.81, 2.95] vs. 2.60 [2.53, 2.67], p < .05). Stratified analysis by separation type and by gender indicated that the association was stronger for child-separation only and for female participants.

Conclusion: Child-separation is an important source of migration-related stress, and the effect is particularly strong for migrant women. Public policies and intervention programs should consider these factors to encourage and facilitate the co-migration of parents with their children to mitigate migration-related stress.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0154252PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4849777PMC
March 2017

Prognostic role of PPAR-γ and PTEN in the renal cell carcinoma.

Int J Clin Exp Pathol 2015 1;8(10):12668-77. Epub 2015 Oct 1.

Department of Urinary Surgery, Huaihe Hospital, Henan University Kaifeng 475000, P. R. China.

Objective: To explore association of peroxisome proliferator-activated receptor gamma (PPAR-γ) and phosphatase and tensin homolog (PTEN) expressions with prognosis of renal cell carcinoma (RCC).

Methods: Our study subjects included 87 RCC tissues, 28 paracarcinoma tissues and 21 normal renal tissues. PPAR-γ and PTEN detection was conducted using immunohistochemistry staining. The association of PPAR-γ and PTEN with the clinical parameters and prognosis of RCC was analyzed. Kaplan-Meier method and Cox's proportional hazards regression model were used for exploring the relation between variables and prognosis.

Results: Among normal renal tissues, para-carcinoma tissues and renal cell carcinomas, positive PPAR-γ expression presented with a progressive tendency (P < 0.001), while positive PTEN expression a degressive tendency (P < 0.001). PPAR-γ expressions were closely related to tumor size, clinical stage and lymph node metastases (all P < 0.05). PTEN expressions were in close association with tumor size, Fuhrman grading, lymph node metastases (all P < 0.05). PPAR-γ expressions were in a negative relation with PTEN expressions (r = -0.417, P < 0.001). Negative PPAR-γ expressions confer a significantly higher overall survival rate than positive PPAR-γ expressions (P = 0.015), while negative PTEN expressions confer a significantly lower overall survival rate than positive PTEN expressions (P = 0.003). Clinical staging, Fuhrman grading, lymph node metastases, PPAR-γ and PTEN were independent prognostic factors for prognosis (all P < 0.05).

Conclusion: PPAR-γ and PTEN expressions are related to the clinical parameters and prognosis of RCC and may be a biomarker for prognosis of RCC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4680401PMC
October 2016

Antibacterial Activity of Stenotrophomonas maltophilia Endolysin P28 against both Gram-positive and Gram-negative Bacteria.

Front Microbiol 2015 24;6:1299. Epub 2015 Nov 24.

College of Life Sciences, Wuhan University Wuhan, China ; Hubei Provincial Cooperative Innovation Center of Industrial Fermentation Wuhan, China.

Maltocin P28 is a phage-tail like bacteriocin produced by Stenotrophomonas maltophilia P28. The ORF8 of maltocin P28 gene cluster is predicted to encode an endolysin and we name it endolysin P28. Sequence analysis revealed that it contains the lysozyme_like superfamily conserved domain. Endolysin P28 has the four consensus motifs as that of Escherichia coli phage lambda gpR. In this study, endolysin P28 was expressed in E. coli BL21 (DE3) and purified with a C-terminal oligo-histidine tag. The antibacterial activity of endolysin P28 increased as the temperature rose from 25 to 45°C. Thermostability assays showed that endolysin P28 was stable up to 50°C, while its residual activity was reduced by 55% after treatment at 70°C for 30 min. Acidity and high salinity could enhance its antibacterial activity. Endolysin P28 exhibited a broad antibacterial activity against 14 out of 16 tested Gram-positive and Gram-negative bacteria besides S. maltophilia. Moreover, it could effectively lyse intact Gram-negative bacteria in the absence of ethylenediaminetetraacetic acid as an outer membrane permeabilizer. Therefore, the characteristics of endolysin P28 make it a potential therapeutic agent against multi-drug-resistant pathogens.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fmicb.2015.01299DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4656821PMC
December 2015

Expression of Robo protein in bladder cancer tissues and its effect on the growth of cancer cells by blocking Robo protein.

Int J Clin Exp Pathol 2015 1;8(9):9932-40. Epub 2015 Sep 1.

Department of Urology, Henan University Huaihe Hospital Kaifeng 475000, China.

This study aimed to detect the expression of Slit signaling protein ligand Robo protein in human bladder cancer and para-carcinoma tissue, and observe the tumor cell survival and growth by inoculating the bladder cancer cells with the blocked signaling protein into the subcutaneous tissue of nude mice. The expression of Robo protein was detected in T24 cells in human bladder uroepithelium carcinoma and cultivated human bladder uroepithelium carcinoma confirmed by pathological diagnosis. The cultivated T24 cells were coated by the protein antibody and human bladder uroepithelium carcinoma T24 tumor-bearing mice model was established. The tumor cell survival and growth were observed in the antibody coating group and non-coating group. The tumor body size was measured. The immunohistochemical detection showed that Robo protein isoforms Robo1 and Robo 4 were expressed in T24 cells of cancer tissues, paracarcinoma tissues and cultured human uroepithelium carcinoma. The expression of Robo1 was significantly higher than that of Robo4 (P<0.05). The cancer cells could be detected in nodular tumor of mice in each group. The volume of the tumor-bearing mice in the nodular tumor of the non-coating group was larger than that of anti-Robol antibody coating group and the difference was statistically significant (P<0.01). There was no significant difference in tumor volume between anti-Robo4 antibody coating group and non-coating group (P>0.05); The difference was statistically significant compared with the anti-Robo1 antibody coating group (P<0.01). In conclusion, Robo protein isoforms Robo1 and Robo4 were expressed in human bladder cancer T24 cells. To block Robo4 signal protein had little effect on the survival and growth of the transplantation tumor and to block Robo1 signal protein would seriously affect the survival and growth of the transplantation tumor, suggesting that Robo1 might play an important role in the growth and metastasis of bladder cancer, and might become a new target for the treatment of human bladder cancer and drug research.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4637787PMC
September 2016

[Development of mobile monitor for risk factor control on chronic disease].

Zhongguo Yi Liao Qi Xie Za Zhi 2013 Nov;37(6):411-3, 420

In order to improve the control rate of risk factors of chronic disease, it is developed a status control method of risk factor and its mobile monitor. The monitor uses 32 bit RISC microprocessor of S3C2410X as a controller based on ARM920T core, and MC35i cellular engine GSM/GPRS supported by SIEMENS as the communication unit. The proving tests show that the physical activity, diet, smoking and alcohol of the controlled people can be controlled using the status control method, and the monitor plays a key role in the method. The conclusion is that status control method and mobile monitor can become an alternation method and technology for the risk factor control of chronic disease.
View Article and Find Full Text PDF

Download full-text PDF

Source
November 2013

[Some perspectives of management in the use of medical devices].

Zhongguo Yi Liao Qi Xie Za Zhi 2011 Jul;35(4):277-9

School of Medicine, Zhejiang University, Hangzhou 310058, China.

The improper selection, management or use of medical devices may lead to a disproportionate rise in the cost of healthcare, which has concerned many countries. Some perspectives of management in the use of medical device have been widely discussed in 1st global forum on medical devices held by the World Health Organization on Thailand in 2010. This paper presents some main perspectives about this.
View Article and Find Full Text PDF

Download full-text PDF

Source
July 2011

[Status and challenges of medical metrology in China].

Zhongguo Yi Liao Qi Xie Za Zhi 2010 Mar;34(2):133-5, 128

School of Medicine, Zhejiang University, Hangzhou 310058.

In recent years, more and more new medical devices appears, among them there are many measurement instruments related to consistency and stability of value, and safety to device. Presently China is facing the health policy reforms and medical quantity management system establishment. The primary duty of the clinical engineering is to ensure security and validity of medical devices, and preventing maintenance included of measurement and safety is important measure for the duty. The paper overviews the status in medical metrology and challenge for health policy reform in China, and gives some suggestions to resolve medical metrology.
View Article and Find Full Text PDF

Download full-text PDF

Source
March 2010
-->