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

Hossain Mohammad Zakir^1, , Md. Nazrul Islam², Murshed Hasan Sarkar³, Amit Kumar Dey³, Ruhul Amin³, Jahanara Khanam⁴, Mele Jesmin¹, Husna Parvin Nur³ and Shaikh M Mohsin Ali¹

¹Department of Applied Chemistry and Chemical Engineering, University of Rajshahi, Rajshahi-6205, Bangladesh

²Department of Applied Chemistry and Chemical Engineering, University of Chittagong, Chittagong-4331, Bangladesh

³Bangladesh Council of Scientific and Industrial Research, Rajshahi, Bangladesh

⁴Department of Biochemistry & Molecular Biology, University of Rajshahi, Rajshahi-6205, Bangladesh

Cite this paper:
Hossain Mohammad Zakir, Md. Nazrul Islam, Murshed Hasan Sarkar, Amit Kumar Dey, Ruhul Amin, Jahanara Khanam, Mele Jesmin, Husna Parvin Nur and Shaikh M Mohsin Ali. Induction of Apoptosis in Ehrlich Ascites Carcinoma Cells Through an Intrinsic Pathway by Ni(II)-benzoin Thiosemicarbazone Complex [Ni(BTSC)₂]. Journal of Cancer Research and Treatment. 2018; 6(2):39-46. doi: 10.12691/jcrt-6-2-3

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.

Keywords:
EAC cells nickel benzoin thiosemicarbazone complex intrinsic pathway ROS caspase inhibitor

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