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首页> 外文期刊>Biology Open >Overexpression of long noncoding RNA GAS5 suppresses tumorigenesis and development of gastric cancer by sponging miR-106a-5p through the Akt/mTOR pathway
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Overexpression of long noncoding RNA GAS5 suppresses tumorigenesis and development of gastric cancer by sponging miR-106a-5p through the Akt/mTOR pathway

机译：长非编码RNA GAS5的过表达通过Akt / mTOR途径使miR-106a-5p海绵化，从而抑制胃癌的发生和发展

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摘要

Long noncoding RNAs (lncRNAs) have emerged as important regulators of human cancers. LncRNA GAS5 (GAS5) is identified as a tumor suppressor involved in several cancers. However, the roles of GAS5 and the mechanisms responsible for its functions in gastric cancer (GC) have not been well documented. Herein, the decreased GAS5 and increased miRNA-106a-5p levels were observed in GC and cell lines. GAS5 level was significantly inversely correlated with miRNA-106a-5p level in GC tissues. Moreover, dual-luciferase reporter and qRT-PCR assays showed that GAS5 bound to miRNA-106a-5p and negatively regulated its expression in GC cells. Functional experiments showed that GAS5 overexpression suppressed GC cell proliferation, migration and invasion capabilities, and promoted apoptosis, while miRNA-106a-5p overexpression inverted the functional effects induced by GAS5 overexpression.In vivo, GAS5 overexpression inhibited tumor growth by negatively regulating miRNA-106a-5p expression. Mechanistic investigations revealed that GAS5 overexpression inactivated the Akt/mTOR pathway by suppressing miRNA-106a-5p expressionin vitroandin vivo. Taken together, our findings conclude the GAS5 overexpression suppresses tumorigenesis and development of gastric cancer by sponging miR-106a-5p through the Akt/mTOR pathway.
机译：长的非编码RNA（lncRNA）已经成为人类癌症的重要调节剂。 LncRNA GAS5（GAS5）被鉴定为与几种癌症有关的肿瘤抑制因子。但是，GAS5的作用及其在胃癌（GC）中起作用的机制尚未得到充分的证明。在本文中，在GC和细胞系中观察到GAS5降低和miRNA-106a-5p水平升高。 GCS组织中GAS5水平与miRNA-106a-5p水平显着负相关。此外，双荧光素酶报告基因和qRT-PCR分析表明GAS5与miRNA-106a-5p结合并对其在GC细胞中的表达负调控。功能实验表明，GAS5的过表达抑制了GC细胞的增殖，迁移和侵袭能力，并促进了细胞凋亡，而miRNA-106a-5p的过表达则逆转了GAS5的过表达所致的功能作用。 -5p表达式。机理研究表明，GAS5过表达通过在体内外抑制miRNA-106a-5p的表达而使Akt / mTOR通路失活。综上所述，我们的研究结果得出结论，GAS5过表达通过Akt / mTOR途径使miR-106a-5p海绵化，从而抑制了胃癌的发生和发展。

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