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Osthole resensitizes CD133+ hepatocellular carcinoma cells to cisplatin treatment via PTEN/AKT pathway

机译:Esthole通过PTEN / AKT途径将CD133 +肝细胞癌细胞恢复为顺铂治疗

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摘要

The population of CD133 positive cancer cells has been reported to be responsible for drug resistance of hepatocellular carcinoma (HCC). However, the potential molecular mechanism by which CD133 HCC cells develop drug resistance is still unclear. In this study, we found that CD133 HepG2 and Huh7 cells were resistant to cisplatin treatment, compared to the CD133 HepG2 and Huh7 cells. However, treatment with osthole, a natural coumarin isolated from umbelliferae plant monomers, was found to resensitize CD133 HepG2 and Huh7 cells to cisplatin treatment. In the mechanism research, we found that treatment with osthole increased the expression of PTEN. As a result, osthole inhibited the phosphorylation of AKT and Bad to decrease the amount of free Bcl-2 in CD133 HepG2 and Huh7 cells. Finally, cisplatin-induced mitochondrial apoptosis was expanded. In conclusion, combination treatment with osthole can resensitize CD133 HCC cells to cisplatin treatment via the PTEN/AKT pathway.
机译:据报道,CD133阳性癌细胞的群体负责肝细胞癌(HCC)的耐药性。然而,CD133 HCC细胞发育耐药性的潜在分子机制仍然不清楚。在这项研究中,与CD133 HepG2和HuH7细胞相比,我们发现CD133 HepG2和Huh7细胞对顺铂治疗耐药。然而,发现与Osthole的治疗是从umbelliferae植物单体中分离的天然香豆素,将CD133 Hepg2和Huh7细胞恢复为顺铂治疗。在机制研究中,我们发现用胞孔治疗增加了PTEN的表达。结果,胞孔抑制AKT的磷酸化,不良,以降低CD133 HepG2和Huh7细胞中的游离Bcl-2的量。最后,扩增了顺铂诱导的线粒体细胞凋亡。总之,用苯甲酰孔的组合处理可以通过PTEN / AKT途径将CD133 HCC细胞转化为顺铂处理。

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