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A‐activated protein kinase is required for cell survival and growth in hela‐s3 cells in vivo
Author(s) -
Song Xuhong,
Huang Dongyang,
Liu Yanmin,
Pan Xiaokang,
Zhang Jing,
Liang Bin
Publication year - 2014
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.1279
Subject(s) - ampk , hela , metformin , cell growth , amp activated protein kinase , protein kinase a , cancer cell , microbiology and biotechnology , cell , apoptosis , cancer research , chemistry , activator (genetics) , kinase , biology , cancer , endocrinology , biochemistry , diabetes mellitus , genetics , gene
Activation of the AMP‐dependent protein kinase (AMPK) is linked to cancer cell survival in a variety of cancer cell lines, particularly under conditions of stress. As a potent activator of AMPK, metformin has become a hot topic of discussion for its effect on cancer cell. Here, we report that AMPK activated by metformin promotes HeLa‐S3 cell survival and growth in vivo . Our results show that metformin inhibited cell proliferation in MCF‐7 cells, but not in LKB1‐deficient HeLa‐S3 cells. Re‐expression of LKB‐1 in HeLa‐S3 cells restored the growth inhibitory effect of metformin, indicating a requirement for LKB‐1 in metformin‐induced growth inhibition. Moreover, AMPK activation exerted a protective effect in HeLa‐S3 cells by relieving ER stress, modulating ER Ca 2+ storage, and finally contributing to cellular adaptation and resistance to apoptosis. Our findings identify a link between AMPK activation and cell survival in HeLa‐S3 cells, which demonstrates a beneficial effect of AMPK activated by metformin in cancer cell, and suggests a discrete re‐evaluation on the role of metformin/AMPK activation on tumor cell growth, proliferation, and on clinical application in cancer therapy. © 2014 IUBMB Life, 66(6):415–423, 2014

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