ArticleScience advances2025
AKR1B10 dictates c-Myc stability to suppress colorectal cancer metastasis via PP2A nitration.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Targeting AKR1C1 overcomes lenvatinib resistance in hepatocellular carcinoma through the STAT3-ABC transporters pathway.Journal of gastrointestinal oncology · 2026Article
- AKR1B10 reprograms neutrophils by histone lactylation to foster immune evasion in KRASJournal of experimental & clinical cancer research : CR · 2026Article
- EV-derived miR-1246 promotes lymph node metastasis in esophageal squamous cell carcinoma through targeting the PPP2CB/NF-κB axis.Frontiers in immunology · 2026Article
- Yi-qi-hua-yu-jie-du Decoction Inhibits Gastric Cancer Progression by Inducing Tumor-Associated Macrophage Polarization via Modulating PP2A Enzyme Activity to Mediate the PI3K/AKT/NF-κB Axis.Journal of inflammation research · 2026Article
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Authors and funding
11 authors.
Funding
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Abstract
Metabolic enzymes, critical for cellular homeostasis, are frequently co-opted in a disease-specific manner to drive cancer progression. Here, we identify aldo-keto reductase family 1 member B10 (AKR1B10), down-regulated in gastrointestinal cancers, as a pivotal metastasis suppressor correlating with improved colorectal cancer (CRC) prognosis. Mechanistically, AKR1B10 activates protein phosphatase 2A (PP2A) by preventing redox-regulated nitration of its B56α subunit, preserving holoenzyme assembly and enabling c-Myc dephosphorylation at serine-62. Loss of AKR1B10 disrupts this pathway, stabilizing c-Myc, which drives integrin signaling and metastatic dissemination in CRC. We further demonstrate that lysine-125 of AKR1B10 is essential for its interaction with PP2A-Cα and B56α nitration, thereby attenuating CRC metastatic aggressiveness. Pharmacological restoration of PP2A activity effectively mitigates metastasis associated with AKR1B10 loss. In addition, c-Myc transcriptionally represses AKR1B10, establishing a feedback loop that sustains its down-regulation and enhances metastatic progression. This study uncovers an antimetastatic mechanism involving AKR1B10-mediated PP2A activation and highlights its potential as a biomarker and therapeutic target.
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