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HuR Stabilizes lnc-Sox5 mRNA to Promote Tongue Carcinogenesis

Lifang Wang1,2#, Shucheng Ye2, Junye Wang2, Zhenfang Gu2, Yanhui Zhang2, Chunmei Zhang2, and Xuezhen Ma3#*

1Qingdao University, 266000 Qingdao, China

2Department of Oncology, The Affiliated Hospital of Jining Medical University, Jining, Shandong, China

3Department of Oncology, The Second Affiliated Hospital of Medical College Qingdao University, Qingdao, Shandong, China; E-mail: maxuezhen1978@hotmail.com, npc_2016@163.com

# These authors contributed equally to this work.

* To whom correspondence should be addressed.

Received August 30, 2016; Revision received October 12, 2016
Long noncoding RNAs (lncRNAs) have been recently regarded as systemic regulators in multiple biological processes including tumorigenesis. In this study, we report an ultra-highly expressed lncRNA, lnc-Sox5, in tongue tumor tissues. The results imply that lnc-Sox5 may play vital role in tongue carcinoma progression. We observed that the growth of Tca8113 cells was suppressed by lnc-Sox5 downregulation. Additionally, lnc-Sox5 knockdown simultaneously increased Tca8113 cell apoptosis, but the cell cycle was arrested. RNA immunoprecipitation suggested that HuR directly bound to and stabilized lnc-Sox5 RNA. Consistently, HuR knockdown reduced the level of lnc-Sox5 in Tca8113 cells. However, overexpression of HuR induced more lnc-Sox5 in Tca8113 cells. Both lnc-Sox5 knockdown and HuR knockdown suppressed Tca8113 cell tumorigenesis in xenograft models. These results suggest that lnc-Sox5, which was stabilized by HuR, could regulate carcinogenesis of tongue cancer and may serve as a predicted target for tongue carcinoma therapies.
KEY WORDS: long non-coding RNA, lnc-Sox5, tongue carcinoma, cell cycle, apoptosis, HuR, RNA immunoprecipitation

DOI: 10.1134/S0006297917040046