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

Abstract

A group of cells exhibit uncontrolled proliferation, invasion, and occasionally metastasis in cancer, a category of disorders. According to statistics, cancer is the second largest cause of mortality in the world. As a result, current cancer research places a strong priority on the discovery and development of novel, effective, and selective anticancer medications. The purpose of this work was to determine the method by which Ehrlich ascites cancer (EAC) cells are inhibited by Co(II)-benzoin thiosemicarbazone complex in Swiss albino mice. DNA fragmentation assays and nuclear morphology observations both supported the induction of apoptosis in EAC cells. The mRNA expression levels of many tumor-related antiapoptotic genes, including B-cell lymphoma 2 (bcl-2), B-cell lymphoma extra-large (bcl-xL), and caspase-8, as well as proapoptotic genes, including p53 or tumor protein, bcl-2 associated X protein (bax), caspase-9, caspase-3, and poly-ADP ribose polymerase (PARP-1) and in vitro effect of caspase inhibitors on EAC cells.   Using 2', 7'- dichlorodihydrofluorescein diacetate (DCFH-DA) staining, reactive oxygen species (ROS) production following Co(BTSC)2 treatment were quantified. The findings of this investigation revealed that the induction of apoptosis by Co(BTSC)2 occurred via an intrinsic mitochondria-mediated ROS-dependent mechanism as opposed to an extrinsic one, and that this intrinsic pathway was controlled by the bcl-2 protein family. As a result, this study offers support for conducting more research to develop novel anticancer drugs.