ML-7 amplifies the quinocetone-induced cell death through akt and MAPK-mediated apoptosis on HepG2 cell line

摘要: The study aims at evaluating the combination of quinocetone and ML-7 in preclinical hepatocellular carcinoma models. To this end, effect on apoptosis induction signaling pathways was analyzed HepG2 cell lines. Here, we report that ML-7, a nontoxic concentration, sensitized cells to quinocetone-induced cytotoxicity. Also, profoundly enhances line. Mechanistic investigations revealed act concert trigger cleavage caspase-8 as well Bax/Bcl-2 ratio up-regulation subsequent Bid, capsases-9 -3. Importantly, weakened Akt pathway activation, but strengthened phosphorylation p-38, ERK JNK. Further treatment activator p-38 inhibitor almost completely abolished ML-7/quinocetone-induced apoptosis. In contrast, JNK aggravated apoptosis, indicating synergism critically depended provoke Akt, against conclusion, rational presents promising approach carcinoma, which warrants further investigation.