Correcting Mitochondrial Complex I Defect in Tumor-Associated Natural Killer Cells Potentiates Immunotherapy for Glioblastoma.
Restoring mitochondrial complex I activity via NDUFA9 enhances natural killer cell function, improving immunotherapy outcomes in glioblastoma patients.
- Why it matters: Glioblastoma remains resistant to many immunotherapies, partly due to impaired NK cell metabolism and function, highlighting the need for targeted metabolic interventions.
- What they did: The study used multiomics profiling and genetic manipulation to identify NDUFA9 as essential for NK cell metabolic fitness, demonstrating that its activation boosts anti-tumor activity.
- The result: Enhancing NDUFA9 activity restored NK cell mitochondrial function and epigenetic regulation, leading to improved immunotherapy efficacy and offering a promising therapeutic target for glioblastoma.