TP53 promotes CMA-dependent metabolic adaptations to suppress cancer.

Cytosolic p53 relieves AMPK-mediated inhibition of chaperone-mediated autophagy (CMA), enabling CMA-dependent degradation of IDH1 and IDH2 in cancer cells.

• Why it matters: CMA is often viewed as predominantly tumor promoting, but its role in cancer metabolism and survival—especially under detachment—remains unclear.
• What they did: Xu et al. show that cytosolic p53 modulates AMPK’s effect on CMA, then track CMA-dependent turnover of IDH1 and IDH2 to assess metabolic and growth outcomes.
• The result: The resulting metabolic shift reduces cancer cell growth and matrix-detached survival, suggesting CMA can suppress tumor behaviors under these conditions.

AI summary of the abstract · may contain errors · not medical advice · read the paper.