H. M. Zakir, Md. Nazrul Islam, M. Sarkar, Amit Kumar Dey, Ruhul Amin, Jahanara Khanam, M. Jesmin, H. Nur, S. M. M. Ali
{"title":"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","authors":"H. M. Zakir, Md. Nazrul Islam, M. Sarkar, Amit Kumar Dey, Ruhul Amin, Jahanara Khanam, M. Jesmin, H. Nur, S. M. M. Ali","doi":"10.12691/jcrt-6-2-3","DOIUrl":null,"url":null,"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.","PeriodicalId":22619,"journal":{"name":"The Journal of Cancer Research","volume":"156 1","pages":"39-46"},"PeriodicalIF":0.0000,"publicationDate":"2018-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Induction of Apoptosis in Ehrlich Ascites Carcinoma Cells Through an Intrinsic Pathway by Ni(II)-benzoin Thiosemicarbazone Complex [Ni(BTSC) 2 ]\",\"authors\":\"H. M. Zakir, Md. Nazrul Islam, M. Sarkar, Amit Kumar Dey, Ruhul Amin, Jahanara Khanam, M. Jesmin, H. Nur, S. M. M. Ali\",\"doi\":\"10.12691/jcrt-6-2-3\",\"DOIUrl\":null,\"url\":null,\"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.\",\"PeriodicalId\":22619,\"journal\":{\"name\":\"The Journal of Cancer Research\",\"volume\":\"156 1\",\"pages\":\"39-46\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2018-05-29\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The Journal of Cancer Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.12691/jcrt-6-2-3\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Journal of Cancer Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.12691/jcrt-6-2-3","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Induction of Apoptosis in Ehrlich Ascites Carcinoma Cells Through an Intrinsic Pathway by Ni(II)-benzoin Thiosemicarbazone Complex [Ni(BTSC) 2 ]
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.