Magnolol induces apoptosis and inhibits ERK-modulated metastatic potential in hepatocellular carcinoma cells

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

研究成果: 雜誌貢獻文章同行評審

12 引文 斯高帕斯(Scopus)

摘要

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-κB) reporter gene, western blotting, and cell invasion assays. Results: Magnolol significantly induced accumulation of sub-G1 phase and caspase-3 activation and inhibited NF-κB 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.
原文英語
頁(從 - 到)1361-1368
頁數8
期刊In Vivo
32
發行號6
DOIs
出版狀態已發佈 - 十一月 1 2018

Keywords

  • Apoptosis
  • Extracellular-signal-regulated kinase
  • Hepatocellular carcinoma
  • Magnolol

ASJC Scopus subject areas

  • 生物化學、遺傳與分子生物學 (全部)
  • 藥理

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