Journal
ONCOTARGET
Volume 8, Issue 3, Pages 4125-4135Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.13670
Keywords
lncRNA XIST; miR-497; MACC1; gastric cancer
Categories
Funding
- National Natural Science Foundation of China [81502576]
- Department of Technology, Gongdong Provinec [2014A020212337, 2015A030313465, 2014A030310045]
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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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