期刊
IN VIVO
卷 32, 期 6, 页码 1361-1368出版社
INT INST ANTICANCER RESEARCH
DOI: 10.21873/invivo.11387
关键词
Magnolol; extracellular-signal-regulated kinase; apoptosis; hepatocellular carcinoma
资金
- Taipei Cathay General Hospital [CGH-MR- A10330, CGH-MR- A106019, CGH-MR-A10407]
- Yilan National Yang-Ming University Hospital [RD2018-019]
Background/Aim: The aim of the present study was to evaluate the anti-cancer effect of magnolol in hepatocellular carcinoma (HCC) cells in vitro. Materials and Methods: HCC SK-Hep1 cells were treated with different concentrations of magnolol or PD98059 [extracellular-signal-regulated kinase (ERK) inhibitor] for 48 h, and then cell viability, apoptosis, signal transduction, expression of anti-apoptotic and metastasis-related proteins, and cell invasion were investigated by [3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] (MTT) assay, flow cytometry, nuclear factor kappa B (NF-kappa B) reporter gene, western blotting, and cell invasion assays. Results: Magnolol significantly induced accumulation of sub-G(1) phase and caspase-3 activation and inhibited NF-kappa B activation, cell invasion, expression of phosphorylated ERK (pERK), anti-apoptotic and metastatic-related proteins. ERK inactivation was required for magnolol-induced inhibition of metastatic potential of SK-Hep1 cells. Conclusion: Taken together, these results indicated that magnolol not only induced apoptosis, but also inhibited ERK-modulated metastatic potential of HCC SK-Hep1 cells.
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