The ruthenium(II)-arene compound RAPTA-C induces apoptosis in EAC cells through mitochondrial and p53-JNK pathways

摘要: An investigation of the molecular mechanism anticancer activity demonstrated by ruthenium(II)–arene compound [Ru(η6-p-cymene)Cl2(pta)] (pta is 1,3,5-triaza-7-phosphaadamantane), termed “RAPTA-C”, in Ehrlich ascites carcinoma (EAC) bearing mice described. RAPTA-C exhibits effective cell growth inhibition triggering G2/M phase arrest and apoptosis cancer cells. Cell cycle associated with increased levels p21 reduced amounts cyclin E. treatment also enhances p53, its triggers mitochondrial apoptotic pathway, as shown change Bax to Bcl-2 ratios, resulting cytochrome c release caspase-9 activation. c-Jun NH2-terminal kinase (JNK) a critical mediator RAPTA-C-induced inhibition. Activation JNK increases significantly during apoptosis. Overall, these results suggest role for p53 EAC-bearing mice. Consequently, significant progression an animal model, which emulates human disease, does so remarkably low general toxicity; hence, has potential clinical application.