5 results on '"YONGHAO NAN"'
Search Results
2. Comprehensive Gene Expression Analysis in NMIBC Using RNA-seq Reveals New Therapy Strategies
- Author
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Xiaoliang Chen, Fuquan Jiang, Chunshu Jia, Ming Liu, Yonghao Nan, Licheng Qu, Qingkuo Kong, Fangfang Hou, Wenshan Luo, Wanli Na, Xuefei Jin, and Jiufeng Tan
- Subjects
NMIBC ,modularization ,WGCNA ,PPI ,biomarker ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Non-muscle invasive bladder cancer (NMIBC) patients often have fewer treatment options, and suffer the progression of disease due to mechanisms that are not clear, as well as due to its diversity. This study was designed to explore the molecular mechanism of bladder cancer through an RNA-seq. In addition to conventional analyses, we also simplified the network through modularization using the WGCNA algorithm, with the help of the topological overlapping matrix and hierarchical cluster tree, which are based on the PPI network of STRING. Furthermore, the hub genes were confirmed through survival analyses in the independent cohorts (n = 431). Among them, 15 genes were significantly associated with poor prognosis. Finally, we validated the results at mRNA and protein level using qRT-PCR, IHC and western blotting. Taken together, our research is important for the prediction, as well as the prospective clinical development of drug targets and biomarkers.
- Published
- 2019
- Full Text
- View/download PDF
3. PKM2 Inhibitor Shikonin Overcomes the Cisplatin Resistance in Bladder Cancer by Inducing Necroptosis
- Author
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Yonghao Nan, Wanli Na, Chunshu Jia, Fangshi Hao, Xiaoliang Chen, Licheng Qu, and Yonggang Wang
- Subjects
Male ,0301 basic medicine ,Thyroid Hormones ,Programmed cell death ,Apoptosis Inhibitor ,Necroptosis ,Antineoplastic Agents ,Apoptosis ,In Vitro Techniques ,PKM2 ,Applied Microbiology and Biotechnology ,03 medical and health sciences ,0302 clinical medicine ,Cell Line, Tumor ,Puma ,medicine ,Humans ,Molecular Biology ,Ecology, Evolution, Behavior and Systematics ,Aged ,Cisplatin ,biology ,Chemistry ,Anti-Inflammatory Agents, Non-Steroidal ,Membrane Proteins ,Cell Biology ,Middle Aged ,biology.organism_classification ,Warburg effect ,030104 developmental biology ,Urinary Bladder Neoplasms ,030220 oncology & carcinogenesis ,Cancer research ,Female ,Carrier Proteins ,Naphthoquinones ,Research Paper ,Developmental Biology ,medicine.drug - Abstract
Cisplatin-based chemotherapy often results in the development of chemo-resistance when used to treat bladder cancer (BC), which is difficult to overcome. Recent data indicate that pyruvate kinase M2 (PKM2), a glycolytic enzyme for Warburg effect, is strongly upregulated in BC, and contributes to the cisplatin resistance in BC. However, the underlying mechanisms remain unclear. In this study, we also found that the expression level of PKM2 is also higher in cisplatin resistant BC cells and tumors. Down-regulation of PKM2 by siRNA or inhibition of PKM2 by shikonin re-sensitized the cisplatin resistant T24 cells. Shikonin and cisplatin together exhibit significantly greater killing effects than when used alone. Interestingly, we found shikonin kills the T24 cisplatin resistant cells by inducing necroptosis, as the cell death could not inhibited by apoptosis inhibitor, z-VAD, but compromised by RIP3 inhibitor, GSK872, or RIP3 siRNA. In contrast, shikonin induced apoptosis in T24 parental cells. We further investigate the underlying mechanism, and found that the dysregulation of Bcl-2 family proteins, including Bcl-2, PUMA, Bax, play an important role in deciding that shikonin kills the BC cells by necroptosis or apoptosis. Collectively, our results suggested that inducing necroptosis is an alternative way to overcome the apoptosis resistant in BC therapy, and orchestrating the regulation of Bcl-2, PUMA, and Bax in BC cisplatin resistant cells may improve the therapy effect of cisplatin in BC tumor.
- Published
- 2018
4. Comprehensive Gene Expression Analysis in NMIBC Using RNA-seq Reveals New Therapy Strategies
- Author
-
Licheng Qu, Fuquan Jiang, Wanli Na, Ming Liu, Fangfang Hou, Chunshu Jia, Jiufeng Tan, Wenshan Luo, Yonghao Nan, Xiaoliang Chen, Xuefei Jin, and Qingkuo Kong
- Subjects
0301 basic medicine ,Cancer Research ,PPI ,RNA-Seq ,Disease ,Computational biology ,Biology ,lcsh:RC254-282 ,03 medical and health sciences ,0302 clinical medicine ,Gene expression ,medicine ,Gene ,Original Research ,NMIBC ,Bladder cancer ,WGCNA ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,medicine.disease ,Blot ,030104 developmental biology ,Oncology ,030220 oncology & carcinogenesis ,Ppi network ,modularization ,Biomarker (medicine) ,biomarker - Abstract
Non-muscle invasive bladder cancer (NMIBC) patients often have fewer treatment options, and suffer the progression of disease due to mechanisms that are not clear, as well as due to its diversity. This study was designed to explore the molecular mechanism of bladder cancer through an RNA-seq. In addition to conventional analyses, we also simplified the network through modularization using the WGCNA algorithm, with the help of the topological overlapping matrix and hierarchical cluster tree, which are based on the PPI network of STRING. Furthermore, the hub genes were confirmed through survival analyses in the independent cohorts (n = 431). Among them, 15 genes were significantly associated with poor prognosis. Finally, we validated the results at mRNA and protein level using qRT-PCR, IHC and western blotting. Taken together, our research is important for the prediction, as well as the prospective clinical development of drug targets and biomarkers.
- Published
- 2019
5. MicroRNA‑613 inhibits proliferation and invasion of renal cell carcinoma cells through targeting FZD7.
- Author
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HAITAO SONG, YONGHAO NAN, XINSHENG WANG, GANG ZHANG, SHI ZONG, and XIANGBO KONG
- Subjects
- *
MICRORNA , *RENAL cell carcinoma , *CELL proliferation , *CANCER invasiveness , *METASTASIS - Abstract
MicroRNAs (miRNAs) have emerged as critical regulators in cancer progression. miR‑613 has been reported as a tumor suppressor gene in many types of human cancers. However, the function of miR‑613 in renal cell carcinoma (RCC) remains unclear. In the present study, the authors aimed to detect the expression of miR‑613 and its function in RCC cell lines. miR‑613 was reported to be significantly downregulated RCC cell lines. Functional analyses demonstrated that overexpression of miR‑613 significantly decreased RCC cell proliferation and invasion. Bioinformatics analysis showed that Frizzled7 (FZD7) was a predicted target of miR‑613, which was verified by dual‑luciferase reporter assay, reverse transcription quantitative‑polymerase chain reaction and western blot analysis. Restoration of FZD7 significantly reversed the suppressive effects of miR‑613 on RCC cell proliferation and invasion. Taken together, the results of the present study indicated that miR‑613 functions as a tumor suppressor that inhibits RCC cell proliferation and invasion by targeting and inhibiting FZD7, providing novel insight into RCC pathogenesis and a potential therapeutic target for RCC. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF
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