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Long intergenic non‐coding RNA TUG1 is overexpressed in urothelial carcinoma of the bladder
Author(s) -
Han Yonghua,
Liu Yuchen,
Gui Yaoting,
Cai Zhiming
Publication year - 2012
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.23264
Subject(s) - cancer research , gene silencing , urothelium , transfection , apoptosis , long non coding rna , urothelial cell , medicine , carcinoma , bladder cancer , biology , rna , gene , pathology , urinary bladder , cancer , genetics
Abstract Background and Objectives Long intergenic non‐coding RNAs (lincRNAs) are a class of non‐coding RNAs that regulate gene expression via chromatin reprogramming. Taurine Up‐regulated Gene 1 (TUG1) is a lincRNA that is associated with chromatin‐modifying complexes and plays roles in gene regulation. In this study, we determined the expression patterns of TUG1 and the cell proliferation inhibition and apoptosis induced by silencing TUG1 in urothelial carcinoma of the bladder. Methods The expression levels of TUG1 were determined using Real‐Time qPCR in a total of 44 patients with bladder urothelial carcinomas. Bladder urothelial carcinoma T24 and 5637 cells were transfected with TUG1 siRNA or negative control siRNA. Cell proliferation was evaluated using MTT assay. Apoptosis was determined using ELISA assay. Results TUG1 was up‐regulated in bladder urothelial carcinoma compared to paired normal urothelium. High TUG1 expression levels were associated with high grade and stage carcinomas. Cell proliferation inhibition and apoptosis induction were observed in TUG1 siRNA‐transfected bladder urothelial carcinoma T24 and 5637 cells. Conclusions Our data suggest that lincRNA TUG1 is emerging as a novel player in the disease state of bladder urothelial carcinoma. TUG1 may have potential roles as a biomarker and/or a therapeutic target in bladder urothelial carcinoma. J. Surg. Oncol. 2013;107:555–559. © 2012 Wiley Periodicals, Inc.