LncRNA NEAT1 promotes gastric cancer progression via miR-1294/AKT1 axis

被引:17
作者
Wu, Dianchao [1 ]
Li, Hui [1 ]
Wang, Junfeng [2 ]
Li, Hua [1 ]
Xiao, Qihai [1 ]
Zhao, Xiaofeng [1 ]
Huo, Zhibin [1 ]
机构
[1] Xingtai Peoples Hosp, Dept Surg Oncol, 16 Hongxing St, Xingtai 054031, Hebei, Peoples R China
[2] Tianjin Med Univ Canc Inst & Hosp, Dept Colorectal Surg, Tianjin, Peoples R China
来源
OPEN MEDICINE | 2020年 / 15卷 / 01期
关键词
NEAT1; gastric cancer; miR-1294; AKT1; PI3K/AKT/mTOR pathway; LONG NONCODING RNA; MIGRATION; INVASION; PROLIFERATION; EXPRESSION; GROWTH; CELLS;
D O I
10.1515/med-2020-0218
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Long non-coding RNAs (lncRNAs) were reported to promote the development of gastric cancer (GC). Nuclear-enriched abundant transcript 1 (NEAT1) played a great role in diverse cancers, but the mechanism of NEAT1 in GC remains indistinct. NEAT1 and AKT1 were distinctly up-regulated and miR-1294 was down-regulated in GC tissues and cells. Cell proliferation and metastasis were refrained but apoptosis was promoted in GC cells after knockdown of NEAT1. NEAT1 negatively regulated miR-1294 expression, and the miR-1294 inhibitor reverted the si-NEAT1-induced effect on GC cells. NEAT1 modulated AKT1 expression through miR-1294, and the si-NEAT1-induced effect was relieved by AKT1. NEAT1 affected phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway via regulating miR-1294 and AKT1. NEAT1 could modulate cell proliferation, apoptosis, and metastasis in GC cells by regulating the PI3K/AKT/mTOR signaling pathway via the miR-1294/ AKT1 axis, showing the great potential for NEAT1 as a valid biomarker in the progression and treatment of GC.
引用
收藏
页码:1028 / 1038
页数:11
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