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Curcumin inhibits the growth of liver cancer stem cells through the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway

机译:姜黄素通过磷脂酰肌醇3-激酶/蛋白激酶B /雷帕霉素信号通路的哺乳动物靶标抑制肝癌干细胞的生长

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摘要

Cancer stem cells are considered as a main cause of cancer recurrence. In the present study, the effects of curcumin on the growth of liver cancer stem cells (LCSCs) were investigated. The proliferation and apoptosis of LCSCs were assessed by MTT assays and flow cytometry. Changes in the expression of apoptosis-related proteins were identified by western blotting. The results of the study demonstrated that curcumin treatment inhibited the growth of LCSCs, induced cell apoptosis, as well as regulated the expression of apoptosis-associated proteins and the release of cytochrome c. Further experiments revealed that treatment with curcumin inhibited that the activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway. Treatment with an activator of PI3K/AKT reversed the curcumin-induced growth inhibition of LCSCs. These results demonstrated that curcumin inhibited the growth of LCSCs through the PI3K/AKT/mTOR signaling pathway. Thus, the present study suggested that curcumin may be a potentially efficient agent in the treatment of liver cancer.
机译:癌症干细胞被认为是癌症复发的主要原因。在本研究中,研究了姜黄素对肝癌干细胞(LCSCs)生长的影响。通过MTT测定和流式细胞术评估LCSC的增殖和凋亡。通过蛋白质印迹法鉴定凋亡相关蛋白表达的变化。研究结果表明姜黄素处理可抑制LCSCs的生长,诱导细胞凋亡,并调节凋亡相关蛋白的表达和细胞色素c的释放。进一步的实验表明,姜黄素治疗可抑制磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(AKT)/哺乳动物雷帕霉素靶标(mTOR)信号通路的激活。用PI3K / AKT活化剂治疗可逆转姜黄素诱导的LCSCs生长抑制。这些结果表明姜黄素通过PI3K / AKT / mTOR信号通路抑制LCSCs的生长。因此,本研究提示姜黄素可能是治疗肝癌的潜在有效药物。

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