PT  - JOURNAL ARTICLE
AU  - LIN-YEN KUAN
AU  - WEI-LUNG CHEN
AU  - JIANN-HWA CHEN
AU  - FEI-TING HSU
AU  - TSU-TE LIU
AU  - WEI-TING CHEN
AU  - KAI-LEE WANG
AU  - WEN-CHANG CHEN
AU  - YU-CHANG LIU
AU  - WEI-SHU WANG
TI  - Magnolol Induces Apoptosis and Inhibits ERK-modulated Metastatic Potential in Hepatocellular Carcinoma Cells
AID  - 10.21873/invivo.11387
DP  - 2018 Nov 01
TA  - In Vivo
PG  - 1361--1368
VI  - 32
IP  - 6
4099  - http://iv.iiarjournals.org/content/32/6/1361.short
4100  - http://iv.iiarjournals.org/content/32/6/1361.full
SO  - In Vivo2018 Nov 01; 32
AB  - 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-G1 phase 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.