ArticleBMC urology2024
m6A reader IGF2BP2 promotes M2 macrophage polarization and malignant biological behavior of bladder cancer by stabilizing NRP1 mRNA expression.
Article in BMC urology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- N6-Methyladenosine RNA Methylation: A Key Regulator in Male Reproductive Disorders and Urological Cancers.The world journal of men's health · 2026Review
- IGF2BP2 Promotes Oral Squamous Cell Carcinoma Progression and Is Associated with MAPK Signaling and Macrophage-Related Immune Features.ACS omega · 2026Article
- Diabetic Kidney Disease Progression Alleviated in Mice by ALKBH5-Mediated UC-MSCs-Derived Exosomes That Inhibit TRAF6 m6A Modification and Promote M2 Macrophage Polarisation.Endocrinology, diabetes & metabolism · 2026Article
- IGF2BP2 Deficiency in Macrophages Impairs Migration, Reprograms Metabolism, and Limits Tumor Progression.International journal of biological sciences · 2026Article
- LOXL1-AS1 suppresses ferroptosis in cervical cancer through m6A-dependent regulation of TFRC.Journal of molecular histology · 2025Article
- IMPlications of IMP2 in RNA Biology and Disease.International journal of molecular sciences · 2025Review
- The role and clinical potential of RNA modifications in bladder cancer.Bladder (San Francisco, Calif.) · 2025Review
- The Emerging Role of IGF2BP2 in Cancer Therapy Resistance: From Molecular Mechanism to Future Potential.International journal of molecular sciences · 2024Review
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Authors and funding
7 authors.
Funding
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Abstract
backgroundInsulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) has been confirmed to play oncogenic role in many cancers. However, the role and mechanism of IGF2BP2 in bladder cancer (BCa) still deserves to be further revealed.
methodsThe mRNA and protein levels of IGF2BP2 and neuronilin-1 (NRP1) were detected by real-time quantitative PCR (RT-qPCR) and western blot. Cell proliferation, apoptosis, migration and invasion were determined using colony formation assay, EdU assay, CCK8 assay, flow cytometry and transwell assay. Xenograft tumor model was conducted to evaluate the role of IGF2BP2 in vivo. THP-1-M0 macrophages were co-cultured with the condition medium (CM) of BCa cells to induce polarization. M2 macrophage polarization was assessed by detecting the mRNA levels of M2 macrophage markers using RT-qPCR and measuring the proportion of M2 macrophage markers using flow cytometry. Moreover, MeRIP and RIP assay were performed to assess m6A level and the interaction between IGF2BP2 and NRP1.
resultsIGF2BP2 and NRP1 were upregulated in BCa tissues and cells. IGF2BP2 knockdown suppressed BCa cell growth and metastasis, as well as inhibited BCa tumor growth. After THP-1-M0 macrophages were co-cultured with the CM of BCa cells, the levels of M2 macrophage markers were markedly enhanced, while this effect was abolished by IGF2BP2 knockdown. IGF2BP2 level was positively correlated with NRP1 level, and it could increase NRP1 mRNA stability. NRP1 overexpression reversed the suppressive effect of IGF2BP2 knockdown on M2 macrophage polarization and BCa cell progression.
conclusionm6A-reader IGF2BP2 enhanced M2 macrophage polarization and BCa cell progression by promoting NRP1 mRNA stability.
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