Our research reveals a dual role for BNIP3 in suppressing HCC, both via autophagic turnover of excess mitochondria and associated lipid droplets to prevent fatty liver disease but also as a tonic inhibitor of mTORC1. The activity of BNIP3 in these processes is subject to regulation by nutrient responsive kinases (ULK1 in particular) linking control of mitochondrial mass and lipid metabolism to nutrient availability, mTOR activity and cell growth. Anticipated findings are potentially paradigm shifting in linking mitochondrial dynamics to mTOR signaling and HCC growth.

2R01CA200310-06

2023-06-01

2028-05-31