Nature子刊：厦门大学陈航姿团队揭示癌细胞抵抗双硫死亡新机制，带来癌症治疗新思路

TL;DR - A Nature Cell Biology paper (Aug 7, 2026) from Chen Hangzi's team at Xiamen University identifies the HSPA9–OGDH–METTL3–NRF2 axis as the mechanism melanoma cells use to escape disulfidptosis under glucose starvation, suggesting a combination-therapy strategy. Note: this item is cancer cell biology, not AI research.

• Disulfidptosis, first defined in 2023 (Gan/Chen, MD Anderson), is glucose-deprivation-induced disulfide-stress cell death; tumor escape from it enables survival in glucose-limited niches.
• Mechanism: TCA-cycle rate-limiting enzyme OGDH generates succinyl-CoA, which succinylates METTL3; succinylated METTL3 recognizes m⁶A marks in the NRF2 mRNA coding region, boosting NRF2 translation and TrxR1 expression to block disulfidptosis.
• HSPA9 is upstream, protecting OGDH from oxidative inactivation during glucose deprivation.
• Translational evidence: combined HSPA9 inhibition plus glucose-uptake blockade suppressed melanoma growth in mice; in patients, HSPA9/OGDH levels inversely correlate with disulfidptosis signatures and associate with poor prognosis.