ArticleNeurochemical research2025
FTO Suppresses Proliferation and Induces Apoptosis of T98G Glioblastoma Cells via N6-methyladenosine Modification of GSTO1.
Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- FTO separation-of-function mutations alter mbioRxiv : the preprint server for biology · 2026Article
- Reader-dependent functional duality of FTO: a context-switching node at the intersection of immune evasion and therapeutic resistance.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most malignant type of glioma with a very poor prognosis. N6-methyladenosine (m6A) is well-documented to be involved in GBM progression, and FTO is a demethylase. GSTO1 is also associated with tumor progression. This study aimed to investigate the impact of FTO and GSTO1 on GBM progression and the regulation of FTO on m6A modification of GSTO1. T98G cell phenotypes including proliferation and apoptosis were analyzed by cell counting kit 8, colony formation assay, and flow cytometry. The regulation of m6A methylation mediated by FTO was evaluated by methylated RNA immunoprecipitation, RNA immunoprecipitation, and dual-luciferase reporter assay. The results showed that FTO expression was downregulated in GBM. Overexpression of FTO inhibited cell proliferation and facilitated apoptosis in vitro. Additionally, GSTO1 expression was elevated in GBM, and knockdown of GSTO1 suppressed cell proliferation and promoted apoptosis and oxidative stress. Moreover, FTO inhibited m6A methylation of GSTO1 and reduced the stability of GSTO1. Overexpression of GSTO1 abrogated T98G cellular processes mediated by FTO. The in vivo experiments showed that FTO inhibited tumor growth by downregulating GSTO1 expression. In conclusion, FTO decelerates GBM progression by inducing apoptosis through suppressing m6A methylation of GSTO1.
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Registered trials
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