Curcumin inhibited hypoxia induced epithelial-mesenchymal transition in hepatic carcinoma cell line HepG2 in vitro.
- Author:
Yuan-hong CHANG
1
;
Mei JIANG
;
Kai-ge LIU
;
Xu-qi LI
Author Information
- Publication Type:Journal Article
- MeSH: Cadherins; metabolism; Carcinoma, Hepatocellular; pathology; Cell Hypoxia; Curcumin; pharmacology; Epithelial-Mesenchymal Transition; Hep G2 Cells; Humans; Hypoxia-Inducible Factor 1, alpha Subunit; metabolism; Liver Neoplasms; pathology; Vimentin; metabolism
- From: Chinese Journal of Integrated Traditional and Western Medicine 2013;33(8):1102-1106
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore effects and possible mechanisms of curcumin on hypoxia induced epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma cell line HepG2.
METHODSHepG2 cells were divided to 3 groups, i.e., the normal control group, the CoCl2 group, and the CoCl2 plus 10 micromol/L curcumin group. The proliferation of HepG2 was determined using MTT assay. The migration of HepG2 was detected by wound healing assay.The mRNA expression of hypoxia-inducible factor-1 (HIF-1alpha) was evaluated with real-time RT-PCR. The protein expressions of HIF-1alpha, epithelial-cadherin (E-cadherin), and vimentin were determined using Western blot.
RESULTSCompared with the normal control group, the proliferation and migration of HepG2 cells under CoCl2-induced hypoxia significantly increased, the expression of HIF-1alpha was up-regulated, and the expression of E-cadherin protein was obviously down-regulated, and the expression of vimentin significantly increased (all P < 0.05). Intervention by curcumin significantly inhibited the proliferation and migration of hypoxic HepG2 cells, and expressions of HIF-1alpha and vimentin decreased, and the expression of E-cadherin was up-regulated, showing statistical difference when compared with those of the CoCl2 group (P < 0.05). There was no statistical difference in HIF-1alpha mRNA expression among the 3 groups (P > 0.05).
CONCLUSIONCurcumin could reverse the proliferation and migration of HepG2 cells under CoCl2-induced hypoxia condition, which might be associated with inhibiting up-regulated expressions of HIF-1alpha protein and EMT.