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首页> 外文期刊>Experimental and therapeutic medicine >Chinese herbal formula QHF inhibits liver cancer cell invasion and migration
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Chinese herbal formula QHF inhibits liver cancer cell invasion and migration

机译:中草药配方QHF抑制肝癌细胞的侵袭和迁移

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The aim of the present study was to observe the effects of the Chinese herbal formula QHF (Q, Qingrejiedu; H, Huoxuehuayu; and F, Fuzhengguben) on the migration and invasion of hepatocellular carcinoma (HCC) HepG2 cells and to elucidate the potential molecular mechanisms involved. HepG2 cells were treated with various concentrations of QHF, and scratch and Transwell (R) migration assays were used to qualitatively analyze differences in the migration and invasion activity of these cells. Extracellular signal-regulated kinase (ERK), p38 and c-Jun N-terminal kinase (JNK) inhibitors were subsequently introduced in order to study the association between QHF and the invasion of HepG2 cells. The protein expression levels of the mitogen-activated protein kinase (MAPK) signaling pathway in HepG2 cells in the presence and absence of QHF were additionally determined using western blot analysis. The results showed that QHF significantly inhibited the proliferation of the HepG2 cells in a concentration-dependent manner, in addition to inhibiting cell movement, which reduced the ability of the cells to invade and migrate. Western blot analysis indicated that the effects of QHF on HCC HepG2 cells after 24 h were to significantly decrease the expression of phosphorylated- (p-) ERK and to increase the expression of p-p38 and p-JNK; however, the total quantity of ERK, p38 and JNK protein remained unchanged. The administration of an inhibitor of ERK altered p38 and JNK expression and promoted the anti-invasion effects of QHF, whereas p38 and JNK inhibitors only partially reversed this effect. The results of the present study indicate, therefore, that QHF is able to inhibit the migratory and invasive activity of HepG2 cells. A possible underlying mechanism involves the activation of the p38 and JNK MAPK signaling pathway and the attenuation of the ERK signaling pathway.
机译:本研究的目的是观察中草药配方QHF(Q,清热解毒; H,活血化瘀; F,扶正骨本)对肝细胞癌(HCC)HepG2细胞迁移和侵袭的影响,并阐明其潜在分子涉及的机制。用各种浓度的QHF处理HepG2细胞,并使用刮擦和Transwell(R)迁移测定法定性分析这些细胞迁移和侵袭活性的差异。随后引入细胞外信号调节激酶(ERK),p38和c-Jun N端激酶(JNK)抑制剂,以研究QHF与HepG2细胞侵袭之间的关系。使用蛋白质印迹分析另外确定在存在和不存在QHF的情况下,HepG2细胞中有丝分裂原激活的蛋白激酶(MAPK)信号通路的蛋白表达水平。结果表明,QHF除抑制细胞运动外,还以浓度依赖性方式显着抑制HepG2细胞的增殖,从而降低了细胞侵袭和迁移的能力。蛋白质印迹分析表明,QHF对HCC HepG2细胞的作用在24 h后显着降低了磷酸化(p-)ERK的表达,并增加了p-p38和p-JNK的表达。然而,ERK,p38和JNK蛋白的总量保持不变。 ERK抑制剂的施用改变了p38和JNK的表达并促进了QHF的抗侵袭作用,而p38和JNK抑制剂仅部分逆转了这种作用。因此,本研究的结果表明,QHF能够抑制HepG2细胞的迁移和侵袭活性。可能的潜在机制涉及p38和JNK MAPK信号通路的激活以及ERK信号通路的减弱。

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