Abstract
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.
Original language | English |
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Pages (from-to) | 1361-1368 |
Number of pages | 8 |
Journal | In Vivo |
Volume | 32 |
Issue number | 6 |
DOIs | |
Publication status | Published - Nov 1 2018 |
Keywords
- Apoptosis
- Extracellular-signal-regulated kinase
- Hepatocellular carcinoma
- Magnolol
ASJC Scopus subject areas
- General Biochemistry,Genetics and Molecular Biology
- Pharmacology