HuR Stabilizes lnc-Sox5 mRNA to Promote Tongue Carcinogenesis

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Lifang Wang^1,2#, Shucheng Ye², Junye Wang², Zhenfang Gu², Yanhui Zhang², Chunmei Zhang², and Xuezhen Ma^3#*

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

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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.

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KEY WORDS: long non-coding RNA, lnc-Sox5, tongue carcinoma, cell cycle, apoptosis, HuR, RNA immunoprecipitation

DOI: 10.1134/S0006297917040046

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