期刊
CANCER LETTERS
卷 382, 期 1, 页码 64-76出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2016.08.015
关键词
UCA1; CREB; miR-196a-5p; Drug resistance; Bladder cancer
类别
Chemoresistance constitutes the major failing of clinical therapy for bladder cancer. However, the molecular mechanisms involved in the chemoresistance of bladder cancer are unclear. Long non-coding RNAs (lncRNAs) have been implicated in chemotherapeutic drug resistance. Urothelial Cancer Associated 1 (UCA1), an lncRNA, is reportedly upregulated in human bladder carcinoma and promotes cancer cell proliferation, migration, invasion, and drug resistance. In the present study, knockdown of UCA1 decreased chemosensitivity to cisplatin/gemcitabine by suppressing cell proliferation and inducing apoptosis, while overexpression of UCA1 increased chemosensitivity in bladder cancer cells. Moreover, UCA1 activated transcription factor CREB which led to miR-196a-5p expression by binding with its promoter. miR-196a-5p induction is involved in UCA1 inhibition of apoptosis induced by cisplatin/gemcitabine via targeting p27(Kip1). These results provide a novel UCA1-CREB-miR-196a-5p paradigm to explain in part how UCA1 functions in cisplatin/gemcitabine resistance, and suggest that UCA1 may be a potential therapeutic target for chemotherapy in bladder cancer. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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