Randomized trial shows MCJ deficiency enhances tumor growth suppression in immunocompetent mice, suggesting a novel metabolic immunotherapy target.
Key Points
This study aims to understand the role of mitochondrial methylation-controlled J protein (MCJ) in colorectal cancer and its influence on tumor metabolism and immune response.
Generated MCJ-deficient cancer cell lines using siRNA.
Compared characteristics of MCJ-deficient cells with MCJ-expressing parental cells.
Conducted transcriptomic and bioinformatic analyses to evaluate MCJ expression impact.
MCJ deficiency led to enhanced mitochondrial respiration and ATP production.
MCJ-deficient tumors showed significantly reduced growth in immunocompetent mice (P<0.05).
Low MCJ expression correlated with higher tumor mutational burden and immune cell infiltration.