1128 INVASIVE BLADDER CANCER CELLS ARE DEFICIENT IN DNA REPAIR AND HAVE MUTATOR PHENOTYPES THAT ARE DUE TO SUPPRESSION OF P63 GENE EXPRESSION

2013 ◽  
Vol 189 (4S) ◽  
Author(s):  
Hyun-Wook Lee ◽  
Hsiang-Tsui Wang ◽  
Mao-wen Weng ◽  
Josephine Kuo ◽  
William C. Huang ◽  
...  
2017 ◽  
Vol 13 (5) ◽  
pp. 2975-2981 ◽  
Author(s):  
Jimin Chen ◽  
Nan Zhang ◽  
Jiaming Wen ◽  
Zhewei Zhang

2020 ◽  
Author(s):  
Shen Pan ◽  
Yunhong Zhan ◽  
Xiaonan Chen ◽  
Bin Wu ◽  
Bitian Liu

Abstract Background T1G3 shows a higher chance of recurrence and progression among early bladder cancer types and the available treatment option is controversial. High recurrence and progression are the problems that need to be explored and solved. Changes in the internal signals of bladder cancer cells and differential genes may be the root cause of these problems. Methods GSE120736, GSE19915, GSE19423, GSE32548 and GSE37815 datasets were obtained from Gene Expression Omnibus (GEO ) to identify differentially expressed genes (DEGs). Bladder cancer transcript data from The Cancer Genome Atlas (TCGA) were clustered into different cell-specific gene sets according to weighted gene co-expression network analysis (WGCNA). Multiple sets of databases were used for gene expression comparison, functional enrichment, and protein interaction analysis, including The Human Protein Atlas, Cancer Dependency Map, Metascape, Gene set enrichment analysis, and DisNor. Results DEGs were obtained through GEO data comparison and intersection. After WGCNA was proven to recognise cell-specific gene sets, candidate DEGs were selected and shown to be specifically expressed in cancer cells. Candidate DEGs were related to mitosis and cell cycle. Further, 12 functional candidate markers were identified from the sequencing data of 30 bladder cancer cell lines. These genes were all up-regulated and previously shown to be closely related to bladder cancer progression. Conclusions Twelve functional genes with specific differential expression in bladder cancer cells were identified. WGCNA can identify the relatively specific expression sets of different cells in bladder cancer with greater tumour heterogeneity, which provides new perspectives for future cancer research.


2014 ◽  
Vol 191 (4S) ◽  
Author(s):  
Hsiang-Tsui Wang ◽  
Hyun-Wook Lee ◽  
Mao-wen Weng ◽  
Josephine Kuo ◽  
William C. Huang ◽  
...  

2011 ◽  
Vol 29 (7_suppl) ◽  
pp. 273-273
Author(s):  
H. Williams

273 Background: Muscle invasive bladder cancer portends a poor long term prognosis. Platinum based therapy is the mainstay of treatment but more effective agents are needed for management of this disease. Heat shock protein 90 (Hsp90) is a ubiquitous protein that has been shown to be overexpressed in tumor cells. It functions as a molecular chaperone responsible for the stability and function of a number of proteins critical to the oncogenic process. 17-(allylamino)-17 demethoxygeldanamycin (17 AAG) is a Hsp90 inhibitor that is currently in phase III trials in several tumor models. The purpose of this study was to evaluate the role of 17 AAG treatment for bladder cancer in vitro. Methods: Seven bladder cancer cell lines representing muscle invasive bladder cancer were treated in the presence and absence of 17 AAG. Both short term and long term treatments were evaluated for their effects on growth, motility and invasion of the cancer cells. Expression of proteins involved in cell growth, survival and metastasis were evaluated with Western blotting. Results: Our data demonstrated that 17 AAG treatment resulted in induction of apoptosis, inhibition of cell cycle progression through inhibition of MAP kinase pathway and cyclin D1 expression. Decreased tumor cell motility and invasion was observed with 17 AAG treatment. Several intracellular signaling pathways involved in cell proliferation, invasion and metastasis were inhibited. Conclusions: Hsp90 inhibition in muscle invasive bladder cancer cells impacts growth, motility and invasiveness by inhibiting numerous intracellular signaling pathways. Taken together, these findings suggest a possible role for Hsp90 inhibitors in bladder cancer tumorigenesis. No significant financial relationships to disclose.


2016 ◽  
Vol 48 (4) ◽  
pp. 1617-1627 ◽  
Author(s):  
XIAOJUAN XIE ◽  
JINGJING PAN ◽  
LIQIANG WEI ◽  
SHOUZHEN WU ◽  
HUILIAN HOU ◽  
...  

2016 ◽  
Vol 480 (3) ◽  
pp. 409-414 ◽  
Author(s):  
Yubai Zhang ◽  
Maya Nolan ◽  
Hiroshi Yamada ◽  
Masami Watanabe ◽  
Yasutomo Nasu ◽  
...  

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