Autophagy protein Ulk1 promotes mitochondrial apoptosis through reactive oxygen species.

摘要: Regardless of rapid progression in the field autophagy, it remains a challenging task to understand cross talk with apoptosis. In this study, we overexpressed Ulk1 HeLa cells and evaluated apoptosis-inducing potential gene presence cisplatin. The gain function showed decline cell viability colony formation cells. Ulk1-overexpressing higher apoptotic attributes by an increase percentage annexin V, escalated expression Bax/Bcl2 ratio, caspase-9, -3/7 activities. Further, reactive oxygen species (ROS) generation was found be much HeLa-Ulk1 than mock group. Scavenging ROS N-acetyl-L-cysteine increased number as well mitochondrial membrane (MMP). Our data that on entering into mitochondria inhibits manganese dismutase activity intensifies superoxide level. Ulk1-triggered autophagy (particularly mitophagy) resulted fall ATP; thus nonmitophagic overwork electron-transport cycle replenish energy demand are inadvertently involved overproduction led present investigation, our results decipher previously unrecognized perspective apoptosis induction key protein may contribute identification its tumor-suppressor properties through dissecting connection among cellular bioenergetics, ROS, MMP.