ArticleCell biology and toxicology2026
ALKBH5/IGF2BP1-mediated m
Article in Cell biology and toxicology, 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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Abstract
backgroundThe upregulation of the ubiquitin ligase TRIM37 is associated with an adverse prognosis in pancreatic ductal adenocarcinoma (PDAC). This study investigates the mechanism and oncogenic consequence of TRIM37 upregulation in PDAC development.
methodsTRIM37 expression was assessed by qPCR and Western blotting. The effects of TRIM37 knockdown and overexpression on cell proliferation, colony formation, stemness capacity was investigated through in vitro assays, and the role in PDAC was evaluated through vivo experiments. RNA immunoprecipitation assay and Actinomycin D assay were performed to detect the mechanism of TRIM37 upregulation. The TRIM37 and RBMX interaction were determined through co-immunoprecipitation and immunofluorescence.
resultsWe identified TRIM37 as a critical oncoprotein in PDAC, and its overexpression was strongly correlated with poor prognosis. As a ubiquitin ligase, TRIM37 targets the tumor suppressor RBMX for proteasomal degradation, promoting glycolytic reprogramming and driving aggressive cancer phenotypes, including enhanced proliferation, migration, and stemness. Furthermore, we found that the ALKBH5-IGF2BP1 axis promotes TRIM37 expression by controlling N6-methyladenosine (m
conclusionsOur findings establish the ALKBH5/IGF2BP1-TRIM37-RBMX signaling axis as a pivotal driver of PDAC progression, highlighting the intersection of m
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