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Amentoflavone Inhibits ERK-modulated Tumor Progression in Hepatocellular Carcinoma .穗花杉双黄酮抑制肝细胞癌中ERK调节的肿瘤进展
In Vivo. 2018 May-Jun;32(3):549-554. doi: 10.21873/invivo.11274.
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Regorafenib inhibits tumor progression through suppression of ERK/NF-κB activation in hepatocellular carcinoma bearing mice.regorafenib 通过抑制 ERK/NF-κB 激活抑制荷肝癌小鼠肿瘤进展。
Biosci Rep. 2018 May 8;38(3). doi: 10.1042/BSR20171264. Print 2018 Jun 29.
3
Assessing the selective therapeutic efficacy of superparamagnetic erlotinib nanoparticles in lung cancer by using quantitative magnetic resonance imaging and a nuclear factor kappa-B reporter gene system.利用定量磁共振成像和核因子 κB 报告基因系统评估超顺磁载厄洛替尼纳米粒在肺癌中的选择性治疗效果。
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Hyperforin Inhibits Cell Growth by Inducing Intrinsic and Extrinsic Apoptotic Pathways in Hepatocellular Carcinoma Cells.金丝桃素通过诱导肝癌细胞的内源性和外源性凋亡途径抑制细胞生长。
Anticancer Res. 2017 Jan;37(1):161-167. doi: 10.21873/anticanres.11301.

厚朴酚诱导肝癌细胞凋亡并抑制ERK调节的转移潜能。

Magnolol Induces Apoptosis and Inhibits ERK-modulated Metastatic Potential in Hepatocellular Carcinoma Cells.

作者信息

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

机构信息

Department of Emergency Medicine, Cathay General Hospital, Taipei, Taiwan, R.O.C.

School of Medicine, Fu Jen Catholic University, Taipei, Taiwan, R.O.C.

出版信息

In Vivo. 2018 Nov-Dec;32(6):1361-1368. doi: 10.21873/invivo.11387.

DOI:10.21873/invivo.11387
PMID:30348689
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6365719/
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-ĸB) reporter gene, western blotting, and cell invasion assays.

RESULTS

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.

CONCLUSION

Taken together, these results indicated that magnolol not only induced apoptosis, but also inhibited ERK-modulated metastatic potential of HCC SK-Hep1 cells.

摘要

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。

材料与方法

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。

结果

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。

结论

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。