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首页> 外文期刊>Biochemical and Biophysical Research Communications >Ghrelin promotes human non-small cell lung cancer A549 cell proliferation through PI3K/Akt/mTOR/P70S6K and ERK signaling pathways
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Ghrelin promotes human non-small cell lung cancer A549 cell proliferation through PI3K/Akt/mTOR/P70S6K and ERK signaling pathways

机译:通过PI3K / AKT / MTOR / P70S6K和ERK信号通路促进人类非小细胞肺癌A549细胞增殖

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摘要

Ghrelin is a gastric acyl-peptide that plays an important role in cell proliferation. In the present study, we explored the role of ghrelin in A549 cell proliferation and the possible molecular mechanisms. We found that ghrelin promotes A549 cell proliferation, knockdown of the growth hormone secretagogue receptor (GHSR) attenuated A549 cell proliferation caused by ghrelin. Ghrelin induced the rapid phosphorylation of phosphatidylinositol 3-kinase (PI3K), Akt, ERK, mammalian target of rapamycin (mTOR) and P7056K. PI3K inhibitor (LY 294002), ERK inhibitor (PD98059) and mTOR inhibitor (Rapamycin) inhibited ghrelin-induced A549 cell proliferation. Moreover, GHSR siRNA inhibited phosphorylation of PI3K, Akt, ERK, mTOR and P70S6K induced by ghielin. Akt and mTOR/P70S6K phosphorylation was inhibited by LY 294002 but not by PD98059. These results indicate that ghrelin promotes A549 cell proliferation via GHSR-dependent PI3K/Akt/mTOR/P70S6K and ERK signaling pathways. (C) 2018 Elsevier Inc. All rights reserved.
机译:Ghrelin是一种胃酰肽,其在细胞增殖中起重要作用。在本研究中,我们探讨了Ghrelin在A549细胞增殖中的作用和可能的分子机制。我们发现Ghrelin促进A549细胞增殖,敲低生长激素促蛋白受体(GHSR)的敲低衰减由Ghrelin引起的A549细胞增殖。 Ghrelin诱导磷脂酰肌醇3-激酶(PI3K),Akt,ERK,哺乳动物靶标的快速磷酸化雷帕霉素(MTOR)和P7056K。 PI3K抑制剂(LY 294002),ERK抑制剂(PD98059)和MTOR抑制剂(雷帕霉素)抑制Ghrelin诱导的A549细胞增殖。此外,GHSR siRNA抑制Ghielin诱导的PI3K,AKT,ERK,MTOR和P70S6K的磷酸化。通过294002抑制AKT和MTOR / P70S6K磷酸化,但不是PD98059。这些结果表明,Ghrelin通过GHSR依赖性PI3K / AKT / MTOR / P70S6K和ERK信号传导途径促进A549细胞增殖。 (c)2018年Elsevier Inc.保留所有权利。

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