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首页> 外文期刊>Journal of Cancer Research and Treatment >Induction of Apoptosis in Ehrlich Ascites Carcinoma Cells Through an Intrinsic Pathway by Ni(II)-benzoin Thiosemicarbazone Complex [Ni(BTSC)2]
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Induction of Apoptosis in Ehrlich Ascites Carcinoma Cells Through an Intrinsic Pathway by Ni(II)-benzoin Thiosemicarbazone Complex [Ni(BTSC)2]

机译：Ni（II）-苯偶姻硫代氨基脲复合物[Ni（BTSC）2]通过内在途径诱导腹水癌细胞的凋亡。

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Cancer is one of the leading causes of morbidity and mortality through worldwide. Globally cancer recognized as the second leading cause of death. Therefore, the discovery and development of new potent and selective anticancer drugs are of high importance in modern cancer research. The objective of this study was to find out the mechanism through which Ni(II)-benzoin thiosemicarbazone complex exerts its antitumor activity against Ehrlich Ascites Carcinoma (EAC) cells bearing swiss albino mice. Induction of apoptosis in EAC cells was confirmed by observation of nuclear morphology and DNA fragmentation assay. The mRNA expression of several apoptotic genes like B-cell lymphoma 2 (bcl-2), B-cell lymphoma extra-large (bcl-xL) caspase-8, and proapoptotic genes p53 or tumor protein, bcl-2 associated X protein (bax), caspase-9, caspase-3 and poly-ADP ribose polymerase (PARP-1) reveal the induction of apoptosis by Ni(BTSC)2 in EAC cell. Inhibition of Ni(BTSC)2 induced apoptosis by Caspase 3 inhibitor treatment affirmed that the induction of intrinsic apoptosis pathway on EAC cells. Reactive Oxygen Species (ROS) generation after Ni(BTSC)2 treatment confirmed that the induction of apoptosis by Ni(BTSC)2 occurred through an ROS-dependent mitochondria-mediated intrinsic pathway rather than an extrinsic pathway. Thus, this study provides evidence to carry out further researches in a way to formulate novel anticancer drugs.
机译：癌症是全世界发病率和死亡率的主要原因之一。全球癌症被认为是第二大死亡原因。因此，新的有效和选择性抗癌药物的发现和开发在现代癌症研究中具有高度重要性。这项研究的目的是找出Ni（II）-安息香素硫半乳糖苷复合物通过其对瑞士白化病小鼠的艾氏腹水癌（EAC）细胞发挥抗肿瘤活性的机制。通过观察核形态和DNA片段化测定证实了EAC细胞凋亡的诱导。几种凋亡基因的mRNA表达，例如B细胞淋巴瘤2（bcl-2），超大型B细胞淋巴瘤（bcl-xL）caspase-8和促凋亡基因p53或肿瘤蛋白，bcl-2相关X蛋白（ bax），caspase-9，caspase-3和聚ADP核糖聚合酶（PARP-1）显示Ni（BTSC）2诱导EAC细胞凋亡。 Caspase 3抑制剂处理对Ni（BTSC）2诱导的凋亡的抑制作用证实了EAC细胞固有的凋亡途径的诱导。 Ni（BTSC）2处理后产生的活性氧（ROS）证实，Ni（BTSC）2诱导细胞凋亡是通过ROS依赖的线粒体介导的内在途径而非外在途径发生的。因此，本研究提供了证据，以制定新的抗癌药物的方式进行进一步的研究。

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