6 results on '"Wenping Zhou"'
Search Results
2. Photoluminescence properties of cerium-doped zinc oxide nanotubes prepared using electrodeposition technique
- Author
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Fang Liu, Wenlong Li, Dan Wu, Wenping Zhou, and Guohong Yun
- Subjects
General Materials Science ,General Chemistry - Published
- 2023
3. MiRNA-363-3p/DUSP10/JNK axis mediates chemoresistance by enhancing DNA damage repair in diffuse large B-cell lymphoma
- Author
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Wenping Zhou, Yuanlin Xu, Jiuyang Zhang, Peipei Zhang, Zhihua Yao, Zheng Yan, Haiying Wang, Junfeng Chu, Shuna Yao, Shuang Zhao, Shujun Yang, Yongjun Guo, Jinxin Miao, Kangdong Liu, Wing C. Chan, Qingxin Xia, and Yanyan Liu
- Subjects
Cancer Research ,DNA End-Joining Repair ,DNA Repair ,JNK Mitogen-Activated Protein Kinases ,Hematology ,Mice ,MicroRNAs ,Oncology ,Doxorubicin ,Drug Resistance, Neoplasm ,Cell Line, Tumor ,Animals ,Dual-Specificity Phosphatases ,Humans ,Mitogen-Activated Protein Kinase Phosphatases ,Lymphoma, Large B-Cell, Diffuse ,DNA Damage - Abstract
Anthracycline-based chemotherapy resistance represents a major challenge in diffuse large B-cell lymphoma (DLBCL). MiRNA and gene expression profiles (n = 47) were determined to uncover potential chemoresistance mechanisms and therapeutic approaches. An independent correlation between high expression of miRNA-363-3p and chemoresistance was observed and validated in a larger cohort (n = 106). MiRNA-363-3p was shown to reduce doxorubicin-induced apoptosis and tumor shrinkage in in vitro and in vivo experiments by ectopic expression and CRISPR/Cas9-mediated knockout in DLBCL cell lines. DNA methylation was found to participate in transcriptional regulation of miRNA-363-3p. Further investigation revealed that dual specificity phosphatase 10 (DUSP10) is a target of miRNA-363-3p and its suppression promotes the phosphorylation of c-Jun N-terminal kinase (JNK). The miRNA-363-3p/DUSP10/JNK axis was predominantly associated with negative regulation of homologous recombination (HR) and DNA repair pathways. Ectopic expression of miRNA-363-3p more effectively repaired doxorubicin-induced double-strand break (DSB) while enhancing non-homologous end joining repair and reducing HR repair. Targeting JNK and poly (ADP-ribose) polymerase 1 significantly inhibited doxorubicin-induced DSB repair, increased doxorubicin-induced cell apoptosis and tumor shrinkage, and improved the survival of tumor-bearing mice. In conclusion, the miRNA-363-3p/DUSP10/JNK axis is a novel chemoresistance mechanism in DLBCL that may be reversed by targeted therapy.
- Published
- 2022
4. Design of an on-line monitoring system for radioactive wastewater
- Author
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Lei Wang, Qin Guoxiu, Wenping Zhou, Xue-Song Zhang, Youning Xu, and Weizhe Li
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Radionuclide ,Waste management ,Health, Toxicology and Mutagenesis ,Continuous monitoring ,Monte Carlo method ,Detector ,Public Health, Environmental and Occupational Health ,010403 inorganic & nuclear chemistry ,01 natural sciences ,Pollution ,Particle detector ,030218 nuclear medicine & medical imaging ,0104 chemical sciences ,Analytical Chemistry ,Semiconductor detector ,03 medical and health sciences ,0302 clinical medicine ,Nuclear Energy and Engineering ,Wastewater ,Measuring instrument ,Environmental science ,Radiology, Nuclear Medicine and imaging ,Spectroscopy ,Nuclear chemistry - Abstract
An on-line monitoring system for radioactive wastewater was designed to discriminate the type and concentration of the radionuclides discharged from nuclear facilities. An HPGe semiconductor was used as the detector in the system for continuous monitoring by pumping wastewater. The minimum detectable activity for 137Cs was 0.4 Bq L−1 after 10 min of measuring wastewater with the system. The system can detect excessive radioactivity in the wastewater and quickly and effectively alert personnel. Based on the experimental measurements and the Monte Carlo simulation, the detection efficiency of the system was calibrated, and an efficiency curve was determined for the energy range from 50 to 2754 keV.
- Published
- 2017
5. The effects of lncRNA MALAT1 on proliferation, invasion and migration in colorectal cancer through regulating SOX9
- Author
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Xihong Zhang, Wenping Zhou, Yanyan Liu, Peipei Zhang, Yuanlin Xu, Xiufeng Hu, Jiuyang Zhang, and Shujun Yang
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0301 basic medicine ,Cell ,Mice, Nude ,Biology ,Metastasis ,lcsh:Biochemistry ,03 medical and health sciences ,0302 clinical medicine ,Cell Movement ,Cell Line, Tumor ,microRNA ,Genetics ,medicine ,Animals ,Gene silencing ,lcsh:QD415-436 ,Molecular Biology ,Genetics (clinical) ,Cell Proliferation ,Mice, Inbred BALB C ,MALAT1 ,lncRNA MALAT1 ,Cell growth ,lcsh:RM1-950 ,Cancer ,SOX9 Transcription Factor ,Cell cycle ,miR-145 ,medicine.disease ,Colorectal cancer ,MicroRNAs ,lcsh:Therapeutics. Pharmacology ,030104 developmental biology ,medicine.anatomical_structure ,030220 oncology & carcinogenesis ,Cancer research ,Molecular Medicine ,Female ,RNA, Long Noncoding ,Colorectal Neoplasms ,SOX9 ,Research Article - Abstract
Background For the study, we determine the potential biomarkers and uncover the regulatory mechanisms of lncRNA MALAT1 / miR-145 / SOX9 axis on the abilities of cell growth and cell metastasis of colorectal cancer. Methods Previously published dataset GSE18105 from GEO database was used for microarray analysis to identify differential-expressed lncRNAs and mRNAs. The miRNA which had targeted relationships with both lncRNA and mRNA was predicted using miRCode and Targetscan. The association between lncRNA and miRNA, miRNA and mRNA was verified using dual-luciferase reporter assay. Expression levels of lncRNA MALAT1, miR-145 and SOX9 were examined by quantitative RT-PCR analysis. The cell viability of two cancer cell lines was compared by CCK-8 assay. Colony formation was hired to detected cell proliferation. The cell cycle distribution and apoptotic cell rate were conducted by flow cytometry assay. Wound healing as well as transwell assay were compare the cell migration and cell invasion respectively among groups. The effect of MALAT1 on colorectal cancer in vivo was constructed by xenograft model. Results Significantly dysregulated lncRNAs and mRNAs were identified by microarray analysis. By experimental verification, MALAT1 and SOX9 were expressed in a high percentage of colorectal cancer tumors and cells, while miR-145 was in a low expression. We also identified miR-145 as a target of MALAT1 and SOX9. MALAT1 played a role in regulating cancer process by functioning as a competing endogenous RNA. Silencing MALAT1 could effectively decrease the expression level of SOX9, thus suppress cell viability and metastasis. Down-regulated MALAT1 could induce resistance of G1 phase in cell cycle, and facilitation of colorectal cancer cell apoptosis. Nude mice injected with cells transfected with si-MALAT1 had smaller tumor on size and weight. Conclusions The regulatory function of lncRNA MALAT1 / miR-145 / SOX9 axis was revealed in colorectal cancer based on bioinformatics analysis. LncRNA MALAT1 could facilitate colorectal cancer cell proliferation, invasion and migration by down-regulating miR-145 and up-regulating SOX9. LncRNA MALAT1 could suppress cell cycle and apoptosis through MALAT1 / miR-145 / SOX9 axis.
- Published
- 2018
6. Genome-wide RNAi screen reveals ALK1 mediates LDL uptake and transcytosis in endothelial cells
- Author
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Michael G. Sugiyama, Cristina M. Ramírez, Michael W. Nagle, Bruno Larrivée, Eon Joo Park, Jan R. Kraehling, Keyang Chen, Warren L. Lee, Noemi Rotllan, Joseph W. Fowler, John H. Chidlow, Anne Eichmann, Roxana Ola, Xinbo Zhang, Carlos Fernández-Hernando, Wenping Zhou, William C. Sessa, Joachim Herz, Kevin Jon Williams, Bo Tao, Monica Y. Lee, Chitra Rajagopal, Ewa Folta-Stogniew, and Leena Kuruvilla
- Subjects
Male ,0301 basic medicine ,Low-density lipoprotein receptor gene family ,Endothelium ,Science ,Activin Receptors, Type II ,General Physics and Astronomy ,Biology ,Genome ,Article ,General Biochemistry, Genetics and Molecular Biology ,Mice ,03 medical and health sciences ,medicine ,Animals ,Humans ,Cloning, Molecular ,Receptor ,Cells, Cultured ,Apolipoproteins B ,Multidisciplinary ,Endothelial Cells ,Biological Transport ,Cholesterol, LDL ,General Chemistry ,Cell biology ,Lipoproteins, LDL ,Rnai screen ,Cholesterol ,030104 developmental biology ,medicine.anatomical_structure ,Transcytosis ,Gene Knockdown Techniques ,LDL receptor ,cardiovascular system ,RNA Interference ,lipids (amino acids, peptides, and proteins) ,Activin Receptors, Type I ,Genome-Wide Association Study ,Lipoprotein - Abstract
In humans and animals lacking functional LDL receptor (LDLR), LDL from plasma still readily traverses the endothelium. To identify the pathways of LDL uptake, a genome-wide RNAi screen was performed in endothelial cells and cross-referenced with GWAS-data sets. Here we show that the activin-like kinase 1 (ALK1) mediates LDL uptake into endothelial cells. ALK1 binds LDL with lower affinity than LDLR and saturates only at hypercholesterolemic concentrations. ALK1 mediates uptake of LDL into endothelial cells via an unusual endocytic pathway that diverts the ligand from lysosomal degradation and promotes LDL transcytosis. The endothelium-specific genetic ablation of Alk1 in Ldlr-KO animals leads to less LDL uptake into the aortic endothelium, showing its physiological role in endothelial lipoprotein metabolism. In summary, identification of pathways mediating LDLR-independent uptake of LDL may provide unique opportunities to block the initiation of LDL accumulation in the vessel wall or augment hepatic LDLR-dependent clearance of LDL., Atherosclerosis is caused by low-density lipoprotein (LDL) buildup in the vessel wall, a process thought to be mediated by LDL receptor alone. Here, the authors show that the endothelium can uptake LDL via ALK1, a TGFβ signalling receptor, suggesting new therapies for blocking LDL accumulation in the vessel wall.
- Published
- 2016
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