Galangin inhibits proliferation of HepG2 cells by activating AMPK via increasing the AMP/TAN ratio in a LKB1-independent manner
Galangin inhibits proliferation of HepG2 cells by activating AMPK via increasing the AMP/TAN ratio in a LKB1-independent manner
复制标题
高良姜素通过以不依赖 LKB1 的方式增加 AMP/TAN 比率来激活 AMPK,从而抑制 HepG2 细胞的增殖
DOI:
10.1016/j.ejphar.2013.08.026
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发表时间:
2013-10-15
影响因子:
5
通讯作者:
Luo, Hui
中科院分区:
文献类型:
--
作者:
Zhang, Haitao;Li, Ning;Luo, Hui
Galangin, a flavonol derived from Alpinia officinarurn Hance and used as food additives in southern China, induces apoptosis and autophagy to suppress the proliferation of HepG2 cells. In this study, we demonstrated that galangin induced autophagy by increasing the ratio of AMP/TAN in HepG2 cells. It stimulated the phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and LKB1, but inhibited the phosphorylation of AKT and mTOR. Inhibition of AMPK activation suppressed the dephosphorylation of mTOR to block galangin-induced autophagy. AMPIC activation by galangin appeared to be independent of the LKB1 signaling pathway because the down-regulation of LKB1 by its siRNA failed to affect galangin-induced autophagy. Collectively, the findings demonstrated a novel mechanism of how galangin induces autophagy via activating AIVIPK in a LKB1-independent manner. The induction of autophagy can thus reflect the anti-proliferation effect of galangin in HCC cells. (C) 2013 Elsevier B.V. All rights reserved