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Toxicology. 2014 Dec 4;326:9-17. doi: 10.1016/j.tox.2014.09.010. Epub 2014 Sep 28.

Galangin suppresses HepG2 cell proliferation by activating the TGF-β receptor/Smad pathway.

Author information

1
Department of Biochemistry and Molecular Biology, Guangdong Medical College, Dongguan, Guangdong 523808, China; Affiliated Hospital of Guangdong Medical College, Zhanjiang, Guangdong 524001, China.
2
Affiliated Hospital of Guangdong Medical College, Zhanjiang, Guangdong 524001, China.
3
Department of Biochemistry and Molecular Biology, Guangdong Medical College, Dongguan, Guangdong 523808, China.
4
Department of Biochemistry and Molecular Biology, Guangdong Medical College, Dongguan, Guangdong 523808, China. Electronic address: taohaizhang@tom.com.
5
Department of Chemistry, Guangdong Medical College, Zhanjiang, Guangdong 524023, China. Electronic address: luohui@gdmc.edu.cn.

Abstract

Galangin can suppress hepatocellular carcinoma (HCC) cell proliferation. In this study, we demonstrated that galangin induced autophagy by activating the transforming growth factor (TGF)-β receptor/Smad pathway and increased TGF-β receptor I (RI), TGF-βRII, Smad1, Smad2, Smad3 and Smad4 levels but decreased Smad6 and Smad7 levels. Autophagy induced by galangin appears to depend on the TGF-β receptor/Smad signalling pathway because the down-regulation of Smad4 by siRNA or inhibition of TGF-β receptor activation by LY2109761 blocked galangin-induced autophagy. The down-regulation of Beclin1, autophagy-related gene (ATG) 16L, ATG12 and ATG3 restored HepG2 cell proliferation and prevented galangin-induced apoptosis. Our findings indicate a novel mechanism for galangin-induced autophagy via activation of the TGF-β receptor/Smad pathway. The induction of autophagy thus reflects the anti-proliferation effect of galangin on HCC cells.

KEYWORDS:

Autophagy; Autophagy-related gene; Galangin; Smad; TGF-β receptor

PMID:
25268046
DOI:
10.1016/j.tox.2014.09.010
[Indexed for MEDLINE]

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