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We have demonstrated for the first time that CEP55 directly regulated RACGAP1 expression, and downregulation of RACGAP1 blocked ccRCC mitotic division at the G1 phase and induced apoptosis. Targeted and spatial metabolomics analyses showed that RACGAP1 disruption altered levels of multiple metabolites and inhibited ccRCC growth by reprogramming fatty acid, nucleotide, and lipid metabolism. Importantly, spatial imaging of metabolites uncovered intratumor metabolic heterogeneity in ccRCC, providing novel insights into the metabolic landscape of this malignancy.
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Li et al. (2025) studied this question.
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