Abstract
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.
Highlights
Galangin (3,5,7-trihydroxyflavone) is a flavonoid derived primarily from the rhizome Alpinia officinarum (Hance)
Our previous study demonstrated that 130 μM galangin induces autophagy in hepatocellular carcinoma cells[5,7,8]
In silent information regulator homolog 1 (SIRT1)-knockdown cells, galangin failed to reduce the acetylation of light chain 3 (LC3) (Fig. 4B). These results suggest that deacetylation of endogenous LC3 by SIRT1 is essential for galangin-induced autophagy in HepG2 cells
Summary
Galangin (3,5,7-trihydroxyflavone) is a flavonoid derived primarily from the rhizome Alpinia officinarum (Hance). The microtubule-associated protein 1 light chain 3 (LC3) is a key regulator of autophagy that controls major steps in the autophagic pathway, such as the growth of autophagic membranes, the recognition of autophagic cargoes, and the fusion of autophagosomes with lysosomes[13,14,15,16]. SIRT1 is an NAD-dependent class III histone deacetylase that plays major roles in regulating gene expression, DNA damage repair, metabolism, tumor development, aging, and autophagy[22,23,24,25,26]. We investigated the autophagy-inducing effect of galangin in HepG2 cells and explored the mechanism by which galangin induces autophagy via the deacetylation of endogenous LC3 by SIRT1
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