Long non-coding RNA XIST promotes cell growth and invasion through regulating miR-497/MACC1 axis in gastric cancer

// Lei Ma 1, 6, * , Yongjian Zhou 2, * , Xiaojun Luo 3 , Hai Gao 4, 5 , Xubin Deng 1 , Yingjie Jiang 2, * 1 Cancer Hospital of Guangzhou Medical University, Guangzhou, China 2 Department of Gastroenterology, the First Hospital of Guangzhou, Guangzhou, China 3 Cancer Center, TCM-Integrated Hospital, Southern Medical University, Guangzhou, China 4 Xiamen Hospital of Traditional Chinese Medicine, Xiamen, China 5 Xiamen Hospital Affiliated to Fujian University of Traditional Chinese Medicine, Xiamen, China 6 Department of Gastroenterology, Guangzhou Medical University, Guangzhou, China * These authors contributed equally to this work Correspondence to: Lei ma, email: leima_01@yeah.net Xiaojun Luo, email: carl@smu.edu.cn Hai Gao, email: hai_gao@126.com Xubin Deng, email: xubindeng@126.com Keywords: lncRNA XIST, miR-497, MACC1, gastric cancer Received: April 20, 2016 Accepted: October 19, 2016 Published: November 28, 2016 ABSTRACT Abnormal expression of long non-coding RNA (lncRNAs) often contributes to unrestricted growth and invasion of cancer cells. LncRNA XIST expression is up-regulated in several cancers, however, its modulatory mechanism in gastric cancer (GC) has not been elucidated. In the present study, we found that XIST expression was significantly increased in GC tissues and cell lines. LncRNA XIST promoted cell cycle progression from the G1 phase to the S phase and protected cells from apoptosis, which contributed to GC cell growth. LncRNA XIST also contributed to GC cell invasion both in vitro and in vivo . We revealed that XIST functioned as competing endogenous RNA to repress miR-497, which controlled its down-stream target MACC1. We proposed that XIST was responsible for GC cell proliferation and invasion and XIST exerted its function through the miR-497/MACC1 axis. Our findings suggested that lncRNA XIST may be a candidate prognostic biomarker and a target for new therapies in GC patients.