IGF2BP1 regulates the malignant progression of intrahepatic cholangiocarcinoma by recognizing the m6A modification of FN1.

Authors

Qirilatu Sa, Xiaodong Wang, Guangpeng Jia, Xidong Wang, Riguga Su, A Sigen

Published in

Arab journal of gastroenterology : the official publication of the Pan-Arab Association of Gastroenterology. Jul 24, 2026. Epub Jul 24, 2026.

Abstract

Although advances have been made in intrahepatic cholangiocarcinoma (ICC) treatment, ICC prognosis remains unsatisfactory. Thus, in-depth exploration of ICC pathogenesis to identify new therapeutic targets is crucial for optimizing treatment strategies.
Acquisition of single-cell sequencing data encompassing ICC tumor tissues and adjacent normal tissues was performed via the GEO database. Key cell populations and genes were screened through cell annotation, differential expression gene analysis, and KEGG enrichment analysis. In constructed in vitro cell models, qPCR and western blot were respectively implemented to capture mRNA and protein expression levels. Cell migration, proliferation, and invasion abilities were assessed via wound healing, EdU, and Transwell invasion assays. RIP assay was implemented to evaluate RNA-protein interactions, and MeRIP-qPCR was employed to detect m6A modification levels on RNA.
Bioinformatics analysis revealed an evident increase in the proportion of cholangiocytes in ICC tumor tissues compared to adjacent normal tissues. Within the IGF2BP1 + Malignant subpopulation, which had the highest malignancy score, the expression of IGF2BP1 and FN1 was significantly upregulated. Cellular experiments demonstrated that IGF2BP1 recognizes the m6A modification on FN1 mRNA, thereby stabilizing its expression. Furthermore, significant enhancement of ICC cell proliferation, migration, and invasion capabilities resulted from IGF2BP1 overexpression, while FN1 knockdown markedly attenuated these promoting effects.
Through recognition of the m6A modification on FN1 mRNA, IGF2BP1 facilitates the proliferative, migratory, and invasive capabilities of ICC cells.

PMID:
42498553
Bibliographic data and abstract were imported from PubMed on 25 Jul 2026.

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