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Long non-coding antisense RNA GAS6-AS1 supports gastric cancer progression via increasing GAS6 expression

Zhang, Peichen, Dong, Qiantong, Zhu, Hua, Li, Shi, Shi, Lingyan, Chen, Xiangjian
Gene 2019 v.696 pp. 1-9
antisense RNA, cell proliferation, disease course, gain-of-function mutation, genes, loss-of-function mutation, non-coding RNA, patients, phenotype, signal transduction, stomach neoplasms, therapeutics, tissues, transcription (genetics)
As one broader class of non-coding RNAs (lncRNAs), non-coding antisense (AS) transcripts are functionally characterized to play pivotal roles in various pathophysiological processes, including tumor biology.In this study, the exact biological functions and regulation mechanisms of GAS6-AS1 in gastric cancer (GC) was examined.The expression of GAS6-AS1 was markedly upregulated in GC tissues and is associated with advanced stage (III + IV) of GC patients. Gain-of-function and loss-of-function experiments showed that GAS6-AS1 promoted cell proliferation, migration, invasion ability in vitro and xenograft tumor growth in vivo by promoting entry into S-phase. The mechanistic investigations showed that GAS6-AS1 can control the expression of its cognate sense gene GAS6 at the transcriptional or translational levels by forming a RNA-RNA duplex, consequently inducing an increase of AXL level and driveling AXL signaling pathway activation.Taken together, our studies indicate that GAS6-AS1 significantly driving the aggressive phenotype in GC through activating its cognate sense gene GAS6, and provides a more complete understanding of GAS6-AS1 as a potential therapeutic target for GC.