Proteomics

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A CHKA–PML autophagy checkpoint enables tumors to evade glutamine starvation

ABSTRACT: CHKA phosphorylates PML at Tyr339 to promote its cytoplasmic localization; cytoplasmic PML then induces WIPI2 SUMOylation at Lys281/283, blocking HUWE1-mediated degradation. Stabilized WIPI2 enhances autophagic flux and supports tumor cell survival under metabolic stress.

ORGANISM(S): Homo Sapiens

SUBMITTER: Mian Wu  

PROVIDER: PXD075116 | iProX | Tue Mar 03 00:00:00 GMT 2026

REPOSITORIES: iProX

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A CHKA-PML autophagy checkpoint enables tumors to evade glutamine starvation.

Wang Ruijie R   Cao Leixi L   He Xianwei X   Thorne Rick Francis RF   Wu Qichen Q   Ding Caoyuan C   Zhang Jinjing J   Li Mengfan M   Shi Zeyuan Z   Dong Xinyi X   Li Jing J   Li Hongxiang H   Gao Suhua S   Li Jinming J   Zhang Xu Dong XD   Jin Lei L   Fan Tianli T   Wu Mian M  

Proceedings of the National Academy of Sciences of the United States of America 20260319 12

Glutamine metabolism is essential for tumor cell proliferation and biosynthesis. However, solid tumors often face chronic glutamine deprivation, and the underlying adaptive mechanisms remain incompletely understood. Here, we show that glutamine scarcity upregulates choline kinase alpha (CHKA), whose monomerization enhances its noncanonical protein kinase activity. CHKA phosphorylates promyelocytic leukemia (PML) at tyrosine 339, promoting its cytoplasmic localization. Notably, this reflects a co  ...[more]