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Galangin Induces Autophagy via Deacetylation of LC3 by SIRT1 in HepG2 Cells

机译:高良姜精通过SIRT1在HepG2细胞中通过LC3的脱乙酰作用诱导自噬。

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Galangin suppresses proliferation and induces apoptosis and autophagy in hepatocellular carcinoma (HCC) cells, but the precise mechanism is not clear. In this study, we demonstrated that galangin induced autophagy, enhanced the binding of SIRT1-LC3 and reduced the acetylation of endogenous LC3 in HepG2 cells. But this autophagy was inhibited by inactivation of SIRT1 meanwhile, galangin failed to reduce the acetylation of endogenous LC3 after SIRT1 was knocked-down. Collectively, these findings demonstrate a new mechanism by which galangin induces autophagy via the deacetylation of endogenous LC3 by SIRT1.
机译:高良姜素抑制肝细胞癌(HCC)细胞的增殖并诱导凋亡和自噬,但确切的机制尚不清楚。在这项研究中,我们证明了高良姜素诱导的自噬,增强SIRT1-LC3的结合并减少HepG2细胞中内源性LC3的乙酰化。但是这种自噬被SIRT1的失活所抑制,而敲除SIRT1后,高良姜精不能降低内源性LC3的乙酰化。总的来说,这些发现证明了高良姜精通过SIRT1使内源性LC3脱乙酰而诱导自噬的新机制。

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