ArticleThe Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology2025
m6A Methylation Regulator RBM15-Mediated Upregulation of ITGBL1 mRNA Stability Aggravates Colon Adenocarcinoma Progression by Remodeling the Tumor Microenvironment.
Article in The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- RNA-binding motif proteins as context-dependent regulators of tumor-immune crosstalk, genome stability, and therapeutic vulnerabilities in cancer.Frontiers in immunology · 2026Review
- RBM15-mediated mFrontiers in cell and developmental biology · 2025Review
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3 authors.
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Abstract
Background/Aims: Colon adenocarcinoma (COAD) is a prevalent malignant tumor of the digestive system. Previous research has indicated that RNA N6-methyladenosine (m6A) methyltransferase RNA-binding motif protein-15 (RBM15) is involved in various cancers. We aimed to investigate the function of RBM15 in COAD progression and its underlying molecular mechanism. Materials and Methods: TIMER and UALCAN databases were applied to analyze the relationship between COAD and Integrin β-like 1 protein (ITGBL1) or RBM15. RT-qPCR and Western blot were used to analyze ITGBL1, M2-type macrophage markers, EMT-related markers, and RBM15 expression. CCK-8, colony formation, and transwell experiments detected cell viability, proliferation, migration, and invasion. The effect of ITGBL1 on COAD tumor growth was examined using a xenograft tumor model. The effects of COAD cells on macrophage polarization and the proliferation and apoptosis of CD8+ T cells were analyzed using flow cytometry analysis. Relationships between RBM15 and ITGBL1 were validated using MeRIP and dual-luciferase reporter assay. Results: ITGBL1 and RBM15 contents were elevated in COAD. ITGBL1 knockdown could hinder COAD cell proliferation, migration, invasion, M2-type macrophage polarization, and lymphocyte immunity. Meanwhile, the lack of RBM15 dampened tumor growth in vivo. Mechanistically, RBM15 could increase ITGBL1 expression by m6A methylation. Conclusion: RBM15 could promote COAD progression by regulating ITGBL1 mRNA stability, providing a promising biomarker and a potential target for COAD.
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