ArticleCell biology and toxicology2025
FTO-mediated the destabilization of RASGRF1 mRNA impedes thyroid cancer progression and suppresses macrophage M2 polarization.
Article in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Integrative multi-omics, machine learning, and experimental validation reveal that TPM1 suppresses M2 macrophage polarization and enhances chemosensitivity in acute myeloid leukemia.Cell biology and toxicology · 2026Article
- Mechanistic insights into ferroptosis in thyroid cancer and its therapeutic implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Review
- Reader-dependent functional duality of FTO: a context-switching node at the intersection of immune evasion and therapeutic resistance.Frontiers in immunology · 2026Review
- Mechanism and therapeutic prospects of ferroptosis regulation through m6A in cancer.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
6 authors.
Funding
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Abstract
backgroundThe guanine nucleotide exchange factor RASGRF1 actively acts in a broad range of human cancers, including thyroid cancer (THCA). This study defined the activity of RASGRF1 in THCA progression and elucidated the m6A modification mechanism governing dysregulation of RASGRF1.
methodsExpression analyses were performed by immunoblotting, immunohistochemistry (IHC) or quantitative PCR. Cell growth was evaluated by colony formation and EdU proliferation assays. Animal experiments tested the function of RASGRF1 in xenograft growth. The conditioned medium (CM) of THCA cells was used to treat THP-1-differentiated macrophages. Cell apoptosis and CD206
resultsRASGRF1 was upregulated in human THCA. RASGRF1 depletion retarded THCA cell growth, motility, invasiveness and promoted cell apoptosis and ferroptosis in vitro, as well as diminished the growth of TPC1 THCA xenograft tumors in vivo. Moreover, RASGRF1 depletion diminished M2 polarization and migration of THP-1-differentiated macrophages. Mechanistically, FTO reduced RASGRF1 mRNA stability via an m6A-dependent mechanism. FTO upregulation suppressed THCA malignant behaviors, promoted cell ferroptosis and reduced macrophage M2 polarization and migration through repression of RASGRF1.
conclusionOur findings suggest that FTO-mediated the instability of RASGRF1 mRNA diminishes THCA-related macrophage M2 polarization and THCA progression. Anti-RASGRF1 strategies may be useful for the treatment of THCA.
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