肿瘤细胞治疗研究
英文原题：Mitochondrial Complex I at the Crossroads of NK cell Dysfunction in Glioblastoma.
Zhou及其同事发现，由NDUFA9介导的线粒体复合物I活性是胶质母细胞瘤中自然杀伤（NK）细胞代谢适应性和抗肿瘤功能的关键决定因素。
Zhou及其同事发现，由NDUFA9介导的线粒体复合物I活性是胶质母细胞瘤中自然杀伤（NK）细胞代谢适应性和抗肿瘤功能的关键决定因素。他们的研究将氧化磷酸化受损与谷氨酰胺依赖性、效应程序的表观遗传抑制以及NK细胞活性丧失联系起来，突出表明线粒体适应性是改善实体瘤细胞免疫治疗的一个可干预轴。参见Zhou等人第1924页的相关文章。
Zhou and colleagues identify mitochondrial complex I activity, mediated through NDUFA9, as a critical determinant of natural killer (NK) cell metabolic fitness and antitumor function in glioblastoma. Their study links impaired oxidative phosphorylation to glutamine dependence, epigenetic repression of effector programs, and loss of NK cell activity, highlighting mitochondrial fitness as an actionable axis for improving cellular immunotherapy in solid tumors. See related article by Zhou et al., p. 1924.
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