ArticleMolecular and cellular biochemistry2025
FOXM1-activated IGF2BP3 promotes cell malignant phenotypes and M2 macrophage polarization in hepatocellular carcinoma by inhibiting ferroptosis via stabilizing RRM2 mRNA in an m6A-dependent manner.
Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Global research status and frontiers on ferroptosis in hepatocellular carcinoma: a comprehensive bibliometric and visualized analysis.Frontiers in immunology · 2025Pooled it
- IGF2BP3 Overexpression Accelerates Osteoarthritis Progression by Promoting Glycolysis via mThe Kaohsiung journal of medical sciences · 2026Article
- Targeting IGF2BP3 in Cancer: From Molecular Structure and Biology to Early Drug Discovery.International journal of molecular sciences · 2026Review
- The role of FOXM1 in tumor immunology: implications for cancer treatment strategies.Human cell · 2026Review
- Integrative bulk and single-cell transcriptome analyses reveal RNA modification-related biomarkers of spinal cord injury.Neural regeneration research · 2026Article
- RNA‑binding proteins as epithelial transcriptome orchestrators in gastric cancer: Immune‑metabolic crosstalk and therapeutic vulnerability (Review).International journal of molecular medicine · 2026Review
- RNF112 mediates immunosuppression to inhibit the proliferation of cervical cancer by Foxm1.Translational cancer research · 2026Article
- PTTG3P-miR-142-5p-IGF2BP3 axis governs ferroptosis in hepatocellular carcinoma.Discover oncology · 2026Article
- RNA modifications in intestinal macrophages: Implications for gut immunity and inflammation.Genes & diseases · 2026Review
- CircRNA-TMEM71 Inhibits Human Aortic Smooth Muscle Cell Ferroptosis and Prevents Aortic Dissection Formation Through IGF2BP3-Mediated Stability of FSP1.Journal of the American Heart Association · 2026Article
- Roles of RNA-binding proteins in macrophage function regulation and immunotherapy.Frontiers in cell and developmental biology · 2026Review
- Mechanism and therapeutic prospects of ferroptosis regulation through m6A in cancer.Frontiers in cell and developmental biology · 2026Review
- Bidirectional regulation between ferroptosis and tumor-associated macrophages: mechanisms, strategies, and therapeutic perspectives.Frontiers in oncology · 2026Review
- IGF2BP3-STAT3-METTL3 axis promotes malignant progression in hepatocellular carcinoma (HCC).Human genomics · 2025Article
- RNA methylation in hepatocellular carcinoma: from metabolic reprogramming and immune escape mechanisms to small molecule inhibitor development.Journal of translational medicine · 2025Review
- MAPK/ERK Signaling in Tumorigenesis: mechanisms of growth, invasion, and angiogenesis.EXCLI journal · 2025Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFerroptosis has a crucial role in human carcinogenesis. N6-methyladenosine (m6A) reader insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) suppresses ferroptosis of hepatocellular carcinoma (HCC) cells. Here, we examined the effects and molecular determinants of IGF2BP3-mediated ferroptosis on malignant behaviors of HCC cells.
methodsFerroptosis was evaluated by measuring the levels of malondialdehyde (MDA), glutathione (GSH), reactive oxygen species (ROS), and lipid ROS. HCC cell malignant phenotypes were evaluated by colony formation assay, wound healing assay, and transwell invasion assay. The CD206
resultsHuman HCC tumors showed increased expression of IGF2BP3 compared with adjacent normal tissues. Disruption of IGF2BP3 promoted cell ferroptosis. Moreover, disruption of IGF2BP3 hindered HCC cell growth, invasiveness, and motility and impeded THP1-derived macrophage M2 polarization and migration by inducing ferroptosis. Additionally, IGF2BP3 disruption repressed xenograft growth in vivo. Mechanistically, IGF2BP3 enhanced RRM2 mRNA stability and elevated its protein expression by reading its m6A modification. Overexpression of RRM2 reversed sh-IGF2BP3-mediated ferroptosis and weakened sh-IGF2BP3-mediated suppression of HCC cell malignant phenotypes and macrophage M2 polarization. Furthermore, IGF2BP3 was a downstream target of FOXM1, and knockdown of FOXM1 induced ferroptosis and inhibited cell malignant phenotypes by downregulating IGF2BP3.
conclusionFOXM1-induced IGF2BP3 upregulation promotes HCC cell malignant behaviors and macrophages M2 polarization by repressing ferroptosis via m6A-dependent regulation of RRM2 mRNA. Targeting FOXM1/IGF2BP3/RRM2 to enhance ferroptosis might be exploited as a potent therapeutic strategy for HCC.
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