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Anticancer effects of 10-hydroxycamptothecin induce apoptosis of human osteosarcoma through activating caspase-3 p53 and cytochrome c pathways

机译:10-羟基喜树碱通过激活caspase-3p53和细胞色素c通路诱导人骨肉瘤凋亡

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摘要

In order to evaluate the anticancer effect of 10-hydroxycamptothecin (HCPT) in terms of inducing the apoptosis of human osteosarcoma cells, its apoptosis-inducing molecular mechanisms were investigated. In the present study, the anticancer effects of HCPT were revealed to result in suppressed cell viability, increased cytotoxicity, the induction of apoptosis and an augmented apoptotic nucleolus of human osteosarcoma cells. MG-63 cells were cultured with HCPT (0, 20, 40 and 80 nM) for 24 and 48 h. An MTT assay and a lactate dehydrogenase assay were used to analyze the anticancer effect of HCPT on cell viability and cytotoxicity in MG-63 cells. MG-63 cell apoptosis, and caspase-9 and caspase-3 activity levels were evaluated using flow cytometry and an ELISA. Western blot analysis was used to detect the protein expression levels of p53, poly (ADP-ribose) polymerase-1 (PARP-1), cytochrome c and B cell lymphoma-2 (Bcl-2) in MG-63 cells. The anticancer effects of HCPT were demonstrated to significantly activate the protein expression of p53, PARP-1 and cytochrome c, and suppress Bcl-2 protein expression and promote the activity of caspase-9 and caspase-3 in human osteosarcoma cells. In conclusion, the anticancer effects of HCPT appear to induce the apoptosis of human osteosarcoma cells through the activation of the caspase-3, p53 and cytochrome c pathways.
机译:为了评价10-羟基喜树碱(HCPT)在诱导人骨肉瘤细胞凋亡方面的抗癌作用,研究了其诱导细胞凋亡的分子机制。在本研究中,HCPT的抗癌作用可导致细胞存活力降低,细胞毒性增加,细胞凋亡诱导和人骨肉瘤细胞凋亡核仁增多。 MG-63细胞与HCPT(0、20、40和80 nM)培养24和48小时。使用MTT测定法和乳酸脱氢酶测定法分析HCPT对MG-63细胞中细胞活力和细胞毒性的抗癌作用。使用流式细胞仪和ELISA评估MG-63细胞凋亡以及caspase-9和caspase-3活性水平。 Western blot分析用于检测MG-63细胞中p53,聚(ADP-核糖)聚合酶-1(PARP-1),细胞色素c和B细胞淋巴瘤2(Bcl-2)的蛋白表达水平。 HCPT的抗癌作用可显着激活人骨肉瘤细胞中p53,PARP-1和细胞色素c的蛋白表达,并抑制Bcl-2蛋白的表达并促进caspase-9和caspase-3的活性。总之,HCPT的抗癌作用似乎通过激活caspase-3,p53和细胞色素c通路来诱导人骨肉瘤细胞凋亡。

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