Kuan Lin-Yen, Chen Wei-Lung, Chen Jiann-Hwa, Hsu Fei-Ting, Liu Tsu-Te, Chen Wei-Ting, Wang Kai-Lee, Chen Wen-Chang, Liu Yu-Chang, Wang Wei-Shu
Department of Emergency Medicine, Cathay General Hospital, Taipei, Taiwan, R.O.C.
School of Medicine, Fu Jen Catholic University, Taipei, Taiwan, R.O.C.
In Vivo. 2018 Nov-Dec;32(6):1361-1368. doi: 10.21873/invivo.11387.
BACKGROUND/AIM: The aim of the present study was to evaluate the anti-cancer effect of magnolol in hepatocellular carcinoma (HCC) cells in vitro.
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.
Magnolol significantly induced accumulation of sub-G 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.
Taken together, these results indicated that magnolol not only induced apoptosis, but also inhibited ERK-modulated metastatic potential of HCC SK-Hep1 cells.
背景/目的:本研究旨在评估厚朴酚对体外培养的肝癌(HCC)细胞的抗癌作用。
用不同浓度的厚朴酚或PD98059[细胞外信号调节激酶(ERK)抑制剂]处理肝癌SK-Hep1细胞48小时,然后通过[3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐](MTT)法、流式细胞术、核因子κB(NF-κB)报告基因、蛋白质印迹法和细胞侵袭实验,研究细胞活力、凋亡、信号转导、抗凋亡和转移相关蛋白的表达以及细胞侵袭情况。
厚朴酚显著诱导亚G期细胞堆积和半胱天冬酶-3激活,并抑制NF-κB激活、细胞侵袭、磷酸化ERK(pERK)、抗凋亡和转移相关蛋白的表达。厚朴酚诱导SK-Hep1细胞转移潜能抑制需要ERK失活。
综上所述,这些结果表明厚朴酚不仅诱导凋亡,还抑制肝癌SK-Hep1细胞中ERK调节的转移潜能。