Long non-coding RNA XIST promotes cell growth and invasion through regulating miR-497/MACC1 axis in gastric cancer
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Lei Ma1,6,*, Yongjian Zhou2,*, Xiaojun Luo3, Hai Gao4,5, Xubin Deng1, Yingjie Jiang2,*
1Cancer Hospital of Guangzhou Medical University, Guangzhou, China
2Department of Gastroenterology, the First Hospital of Guangzhou, Guangzhou, China
3Cancer Center, TCM-Integrated Hospital, Southern Medical University, Guangzhou, China
4Xiamen Hospital of Traditional Chinese Medicine, Xiamen, China
5Xiamen Hospital Affiliated to Fujian University of Traditional Chinese Medicine, Xiamen, China
6Department of Gastroenterology, Guangzhou Medical University, Guangzhou, China
*These authors contributed equally to this work
Lei ma, email: firstname.lastname@example.org
Xiaojun Luo, email: email@example.com
Hai Gao, email: firstname.lastname@example.org
Xubin Deng, email: email@example.com
Keywords: lncRNA XIST, miR-497, MACC1, gastric cancer
Received: April 20, 2016 Accepted: October 19, 2016 Published: November 28, 2016
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.
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