柠檬烯和BEZ 235诱导COLO-320和HCT-116结肠癌细胞凋亡

Raja Ratna Reddy Yakkanti, Manisha Singh, V. Kabra, P. C. Sekhar, K. SreejaVamsi, B. Reddy, S. Ramamoorthy, C. Reddy
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引用次数: 0

摘要

不受调控的细胞凋亡是许多癌症的标志,因此细胞凋亡途径的每一个缺陷都可能成为癌症治疗的潜在靶点。柠檬烯的抗癌机制可能是多因素的。然而,在一些临床前研究中,诱导癌细胞凋亡被认为是主要的机制。因此,我们决定在COLO-320和HCT-116结肠癌细胞中研究凋亡在柠檬烯和BEZ235联合抗肿瘤活性中的作用。通过DAPI染色检测凋亡细胞的荧光显微镜检查,估计caspase活性,Bcl-2家族蛋白以及流式细胞术分析细胞周期。结果表明,两种药物均诱导细胞凋亡,表现为caspases活性升高,Bcl-2家族促凋亡蛋白和抗凋亡蛋白显著改变,促进细胞凋亡和细胞周期阻滞于G1期。综上所述,柠檬烯和BEZ发挥抗癌活性是通过诱导凋亡介导的线粒体介导的CRC细胞内在死亡途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Limonene and BEZ 235 induce apoptosis in COLO-320 and HCT-116 colon cancer cells
Deregulated apoptosis is the hall mark of many cancers, therefore every defect in apoptosis pathway could be a potential target for cancer treatment.The anticancer mechanism of limonene could be multifactorial. However, induction of apoptosis in cancer cells is proposed as the predominant mechanism in several of preclinical studies. Therefore, we determined to investigate the role of apoptosis in the anticancer activity of limonene and BEZ235 combination in COLO-320 and HCT-116 colon cancer cells. Cells after treatments were assessed for apoptosis by DAPI staining for fluorescent microscopic examination of apoptotic cells, estimation of caspases activities, Bcl-2 family proteins in addition to cell cycle analysis by flowcytometry. Results show that both drugs induced apoptosis as demonstrated by increased caspases activity, significant alterations in pro and anti-apoptotic proteins of Bcl-2 family in promoting apoptosis and cell cycle arrest at G1 phase. Over all, it is indicated that limonene and BEZ exerted anticancer activity is mediated through induction of apoptosis involving mitochondria mediated intrinsic death pathway in the selected CRC cells.
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