TY - JOUR
T1 - Magnolol induces apoptosis and inhibits ERK-modulated metastatic potential in hepatocellular carcinoma cells
AU - Kuan, Lin Yen
AU - Chen, Wei Lung
AU - Chen, Jiann Hwa
AU - Hsu, Fei Ting
AU - Liu, Tsu Te
AU - Chen, Wei Ting
AU - Wang, Kai Lee
AU - Chen, Wen Chang
AU - Liu, Yu Chang
AU - Wang, Wei Shu
N1 - Funding Information:
The present study was supported by the Taipei Cathay General Hospital (grant no. CGH-MR-A10330, CGH-MR-A106019, CGH-MR-A10407), the Yilan National Yang-Ming University Hospital (grant no. RD2018-019) The Authors acknowledge the technical services provided by Clinical Medicine Research Laboratory of National Yang-Ming University Hospital and Translational Laboratory.
Publisher Copyright:
© 2018 Institute of Electrical and Electronics Engineers Inc. All rights reserved.
PY - 2018/11/1
Y1 - 2018/11/1
N2 - 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.
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-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.
KW - Apoptosis
KW - Extracellular-signal-regulated kinase
KW - Hepatocellular carcinoma
KW - Magnolol
KW - Apoptosis
KW - Extracellular-signal-regulated kinase
KW - Hepatocellular carcinoma
KW - Magnolol
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U2 - 10.21873/invivo.11387
DO - 10.21873/invivo.11387
M3 - Article
C2 - 30348689
AN - SCOPUS:85055155259
SN - 0258-851X
VL - 32
SP - 1361
EP - 1368
JO - In Vivo
JF - In Vivo
IS - 6
ER -
