ArticleJournal of bone oncology2025
RGS1 stabilized by METTL3-mediated m6A modification promotes the tumorigenicity and macrophage M2 polarization in osteosarcoma.
Article in Journal of bone oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Decoding osteosarcoma pathogenesis: the pivotal influence of mEpigenetics · 2026Review
- Exosomal delivery of METTL3 promotes M1 macrophage polarization by inducing miR-155-5p maturation via m6A modification.Annals of medicine · 2026Article
- METTL3-mCurrent medical science · 2026Article
- Deciphering the malignant synergy: metabolic reprogramming, epigenetic circuitry, and niche remodeling in osteosarcoma-macrophage crosstalk.Frontiers in immunology · 2026Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Regulators of G-protein signaling 1 (RGS1) has been reported to be involved in immune cell regulation in many cancer types. However, the specific role and mechanism in osteosarcoma (OS) progression and macrophage activation remain unclear. Methods: Levels of mRNA and protein were examined using qRT-PCR and western blotting. Transwell assay, wound healing assay, EdU assay and flow cytometry were used to investigate OS cell invasion, migration, proliferation and apoptosis. Xenografts in mice were established for in vivo assay. Macrophage M2 polarization was evaluated by detecting CD206 + macrophages by flow cytometry. ELISA analysis detected IL-6 and TGF-β1 levels. Methylated RNA immunoprecipitation assay was applied to explore the specific binding of RGS1 and METTL3 (methyltransferase-like 3). Results: RGS1 was highly expressed in OS tissues and cells. The silencing of RGS1 suppressed OS cell invasion, migration, growth and impaired immune response by inhibiting macrophage M2 polarization and M2 macrophage-mediated release of IL-10 and TGF-β1. Mechanistically, METTL3 promoted RGS1 m6A modification and stabilized its expression. METTL3 deficiency also inhibited OS cell invasion, migration, growth and macrophage M2 polarization, while these effects could be abolished by RGS1 overexpression. Besides that, IL-10 elevation induced by M2 macrophages promoted OS cell oncogenic phenotypes. Conclusion: METTL3 stabilized RGS1 mRNA in an m6A-dependent manner to promote the tumorigenicity and macrophage M2 polarization in osteosarcoma, suggesting a novel insight into the therapy of osteosarcoma.
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