Abstract Title:

Magnolol Induces Apoptosis and Inhibits ERK-modulated Metastatic Potential in Hepatocellular Carcinoma Cells.

Abstract Source:

In Vivo. 2018 Nov-Dec;32(6):1361-1368. PMID: 30348689

Abstract Author(s):

Lin-Yen Kuan, Wei-Lung Chen, Jiann-Hwa Chen, Fei-Ting Hsu, Tsu-Te Liu, Wei-Ting Chen, Kai-Lee Wang, Wen-Chang Chen, Yu-Chang Liu, Wei-Shu Wang

Article Affiliation:

Lin-Yen Kuan


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-ĸB) reporter gene, western blotting, and cell invasion assays.

RESULTS: Magnolol significantly induced accumulation of sub-Gphase and caspase-3 activation and inhibited NF-ĸB 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.

Study Type : In Vitro Study

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