ArticleMolecules (Basel, Switzerland)2025
β2-Chimaerin Deficiency Favors Polyp Growth in the Colon of Apc
Article in Molecules (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
A Rho-GTPases are pivotal regulators of key cellular processes implicated in colorectal cancer (CRC) progression, yet the roles of their regulatory proteins, particularly GTPase-activating proteins (GAPs), remain poorly understood. This study focuses on β2-chimaerin, a Rac1-specific GAP, in Apc-driven tumorigenesis using the ApcMin/+ mouse model. We demonstrate that β2-chimaerin deficiency selectively promotes the growth of colonic polyps without influencing small intestinal polyp formation. Mechanistically, β2-chimaerin loss is associated with enhanced ERK phosphorylation, while canonical Wnt/β-catenin and E-cadherin pathways remain unaffected, suggesting its specific involvement in modulating proliferative signaling in the colon. Consistent with its tumor-suppressive role, bioinformatics analyses reveal that low β2-chimaerin expression correlates with poor prognosis in CRC patients. This study expands the understanding of Rho-GTPase regulatory mechanisms in intestinal tumorigenesis, providing a basis for future therapeutic strategies targeting Rho-GTPase pathways in CRC.
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