Nature子刊：浙江大学易聪/朱贵欣/孙启明合作发现肿瘤兼顾生长与存活的“代谢-自噬检查点”

TL;DR - A Zhejiang University team (Yi Cong, Zhu Guixin, Sun Qiming) reports in Nature Cell Biology (July 29, 2026) that the glycolytic enzyme PGAM1 doubles as a "metabolic–autophagy checkpoint," directly initiating autophagy independently of its catalytic activity. It matters because it links growth-promoting metabolism to stress survival and identifies a dual-function node that tumors hijack.

• PGAM1 acts as a molecular scaffold recruiting PI3K complex I to phagophore assembly sites, triggering autophagosome formation; this role is genetically required, evolutionarily conserved (shown in both yeast and mammalian systems), and functionally separable from glycolysis.
• The autophagy function is regulated by Atg1/ULK1-mediated phosphorylation, which strengthens Atg14 binding under nutrient starvation.
• In cancer, PGAM1 upregulation simultaneously boosts glycolytic flux and autophagic capacity; disrupting either function significantly suppresses tumor growth, framing PGAM1 as a homeostatic checkpoint co-opted to drive proliferation and stress resistance.
• Note: the item is a WeChat science-media write-up of the paper (link: nature.com/articles/s41556-026-02034-3); no quantitative data beyond the qualitative claims above is provided.