Induction of Apoptosis in Ehrlich Ascites Carcinoma Cells Through an Intrinsic Pathway by Ni(II)-benzoin Thiosemicarbazone Complex [Ni(BTSC) 2 ]

H. M. Zakir, Md. Nazrul Islam, M. Sarkar, Amit Kumar Dey, Ruhul Amin, Jahanara Khanam, M. Jesmin, H. Nur, S. M. M. Ali
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引用次数: 1

Abstract

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.
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Ni(II)-苯甲酸硫代氨基脲配合物[Ni(BTSC) 2]通过内在途径诱导埃利希腹水癌细胞凋亡
癌症是全世界发病率和死亡率的主要原因之一。癌症是全球公认的第二大死亡原因。因此,发现和开发新的强效和选择性抗癌药物在现代癌症研究中具有重要意义。本研究旨在探讨镍(II)-苯并苯甲酸硫代氨基脲配合物对瑞士白化病小鼠埃利希腹水癌(EAC)细胞的抗肿瘤作用机制。通过细胞核形态观察和DNA片段化实验证实了其诱导EAC细胞凋亡的作用。凋亡基因如b细胞淋巴瘤2 (bcl-2)、b细胞淋巴瘤特大(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和多adp核糖聚合酶(PARP-1) mRNA表达揭示了Ni(BTSC)2诱导EAC细胞凋亡。Caspase 3抑制剂对Ni(BTSC)2诱导的细胞凋亡的抑制作用证实了内源性凋亡途径对EAC细胞的诱导作用。Ni(BTSC)2处理后活性氧(ROS)的产生证实了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不是外部途径发生的。因此,本研究为进一步研究新型抗癌药物的配方提供了依据。
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