Ghrelin promotes human non-small cell lung cancer A549 cell proliferation through PI3K/Akt/mTOR/P70S6K and ERK signaling pathways

被引：35
|
作者：
Zhu, Jianhua [1 ]
Yao, Jianfeng [2 ]
Huang, Rongfu [3 ]
Wang, Yueqin [1 ]
Jia, Min [1 ]
Huang, Yan [1 ]
机构：
[1] HUST, Tongji Med Coll, Wuhan Hosp 1, Lab Clin Immunol, 215 Zhongshan Dadao, Wuhan 430022, Hubei, Peoples R China
[2] Quanzhou Maternal & Child Hlth Care Hosp, Quanzhou, Fujian, Peoples R China
[3] Fujian Med Univ, Affiliated Hosp 2, Quanzhou, Fujian, Peoples R China
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2018年 / 498卷 / 03期
基金：
中国国家自然科学基金;
关键词：
Ghrelin; A549; cell; Proliferation; GHSR; PI3K/AktimTOR/P70S6K; ERK; SECRETAGOGUE RECEPTOR; IN-VITRO; AUTOCRINE PATHWAY; PROSTATE-CANCER; EXPRESSION; HORMONE; GROWTH; TUMORS; AXIS; LINES;
D O I：
10.1016/j.bbrc.2018.03.031
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
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.
引用
收藏
页码：616 / 620
页数：5
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