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Chinese Journal of Integrated Traditional and Western Medicine ; (12): 1102-1106, 2013.
Article in Chinese | WPRIM | ID: wpr-359247

ABSTRACT

<p><b>OBJECTIVE</b>To explore effects and possible mechanisms of curcumin on hypoxia induced epithelial-mesenchymal transition (EMT) in hepatocellular carcinoma cell line HepG2.</p><p><b>METHODS</b>HepG2 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.</p><p><b>RESULTS</b>Compared 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).</p><p><b>CONCLUSION</b>Curcumin 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.</p>


Subject(s)
Humans , Cadherins , Metabolism , Carcinoma, Hepatocellular , Pathology , Cell Hypoxia , Curcumin , Pharmacology , Epithelial-Mesenchymal Transition , Hep G2 Cells , Hypoxia-Inducible Factor 1, alpha Subunit , Metabolism , Liver Neoplasms , Pathology , Vimentin , Metabolism
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