ArticleNon-coding RNA research2025
Upregulation of circGDI2 inhibits tumorigenesis by stabilizing the expression of RNA m6A demethylase FTO in oral squamous cell carcinoma.
Article in Non-coding RNA research, 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.
- Circular RNAs in Oral Squamous Cell Carcinoma: A Systematic Review of Emerging Diagnostic and Prognostic Biomarkers.European journal of dentistry · 2026Article
- The regulatory role of circGDI2 in hepatocellular carcinoma proliferation and glycolysis with the involvement of m6A modification.Non-coding RNA research · 2026Article
- Dynamic modifications of circular RNAs drive oncogenesis.Epigenomics · 2025Review
- Reciprocal regulation between m6 A modifications and non-coding RNAs: emerging roles in cancer therapeutic resistance.Discover oncology · 2025Review
- Competing endogenous RNAs network dysregulation in oral cancer: a multifaceted perspective on crosstalk and competition.Cancer cell international · 2024Review
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Oral squamous cell carcinoma (OSCC) is a malignant tumour that is difficult to identify and prone to metastasis and invasion. Circular RNAs (circRNAs) are important cancer regulators and can be used as potential biomarkers. However, OSCC-related circRNAs need to be further explored. We investigated the role of circGDI2 in OSCC and explored its downstream regulatory mechanisms. Methods: Quantitative real-time PCR was used to detect the expression levels of circGDI2 and fat mass and obesity-associated protein (FTO) in cells. Lentiviral transfection was used to construct stable circGDI2 overexpressing cells for subsequent cell function tests. RNA pull-down, RNA Immunoprecipitation (RIP), western blotting, and protein stability assays were conducted to detect circGDI2 binding proteins and their functions. CCK8, Transwell, and wound healing assays were used to verify cell functions after overexpressing circGDI2 or suppressing FTO expression. Animal experiments were performed to verify the results Results: The expression of circGDI2 was markedly decreased in both OSCC cell lines and patient tissues. Overexpression of circGDI2 in OSCC cell lines led to decreased proliferation, migration, and invasion abilities. Knockdown of circGDI2 showed the opposite trend. CircGDI2 has been validated to interact with the FTO protein within cells, as evidenced by mass spectrometry and RIP assays. This interaction was found to prevent the degradation of the FTO protein. Dot blot analysis showed a reduction in N6-methyladenosine (m6A) modification after circGDI2 overexpression. Reduced FTO levels reversed the inhibitory effects of circGDI2 overexpression on cell proliferation, migration, and invasion Conclusions: CircGDI2 functions as a tumour suppressor by binding to the FTO protein to reduce RNA m6A modification levels and ultimately inhibit proliferation and migration in OSCC cells. This study indicates the potential use of circGDI2 as a new target for the prevention and treatment of OSCC.
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