ArticleGastroenterology report2026
GIPC2 suppresses colorectal cancer progression via regulation by UBA1-mediated ubiquitination.
Article in Gastroenterology report, 2026. 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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7 authors.
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Abstract
Background: Colorectal cancer (CRC) constitutes a major worldwide cancer challenge, characterized by consistently increasing numbers of new cases and deaths. GIPC2, a molecule with context-dependent regulatory functions across cancers, remains poorly characterized in CRC. This study aims to investigate the biological functions and underlying molecular mechanisms of GIPC2 in colorectal carcinogenesis and progression. Methods: GIPC2 expression in CRC tissues and cell lines was evaluated utilizing the Cancer Genome Atlas (TCGA) data, western blotting, and immunohistochemistry. The proliferative capacity of cells was assessed by Cell Counting Kit-8 (CCK-8) together with colony-formation assays, and migratory and invasive behaviors were measured using transwell assays combined with analyses of epithelial-mesenchymal transition markers. Protein interactions among UBA1, TRIM21, and GIPC2 were examined by mass spectrometry, co-immunoprecipitation, and immunofluorescence. Results: GIPC2 expression was downregulated among both CRC cell lines and clinical tissue samples, and low GIPC2 levels were associated with poor patient prognosis. Functional analyses showed that GIPC2 suppressed CRC proliferation, migration, and invasion. Mechanistically, UBA1 binds to GIPC2 and, together with TRIM21, catalyzed the assembly of K48-specific ubiquitin chains and subsequent proteasome-dependent breakdown of GIPC2, thereby enhancing PI3K/AKT signaling. Conclusion: Our findings identified GIPC2 as a previously uncharacterized tumor suppressor in CRC and revealed a previously unrecognized UBA1-GIPC2 axis that governs proteasome-mediated regulation of tumor progression. These results provide new mechanistic insight and suggest potential therapeutic targets for CRC treatment.
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