ArticleEpigenetics2023
FTO promotes proliferation and migration of bladder cancer via enhancing stability of STAT3 mRNA in an m6A-dependent manner.
Article in Epigenetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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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
11 citing papers in PubMed, 10 citations in OpenAlex.
- Reader-dependent functional duality of FTO: a context-switching node at the intersection of immune evasion and therapeutic resistance.Frontiers in immunology · 2026Review
- mFrontiers in cell and developmental biology · 2026Review
- The mMolecular biomedicine · 2025Review
- Functions of Tomato (International journal of molecular sciences · 2025Article
- TTC7B triggers the PI4KA-AKT1-RXRA-FTO axis and inhibits colon cancer cell proliferation by increasing RNA methylation.International journal of biological sciences · 2025Article
- Comment onInternational journal of biological sciences · 2025Article
- The impact of METTL3 on bladder cancer through mFrontiers in oncology · 2025Review
- The role and clinical potential of RNA modifications in bladder cancer.Bladder (San Francisco, Calif.) · 2025Review
- Insights into the mCell & bioscience · 2024Review
- Article
- Recent advances of m6A methylation in skeletal system disease.Journal of translational medicine · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N6-Methyladenosine (m6A) plays a key role in the occurrence and development of various cancers. Fat mass and obesity-associated protein (FTO) was is involved in multiple cancers owing to its demethylase activity, and the molecular mechanism underlying FTO-promoted bladder cancer proliferation and migration via the regulation of RNA stability requires further investigation. In the present study, FTO was upregulated in bladder cancer and related to poor prognosis. Gain- and loss-of-function experiments showed that the upregulation of FTO promoted bladder cancer proliferation and migration. Mechanistic studies showed that FTO enhanced the stability of signal transducer and activator of transcription 3 (STAT3) mRNA in an m6A-dependent manner, thereby increasing STAT3 expression, which subsequently promoted P-STAT3 expression and activated STAT3 signalling pathway. Overall, this study revealed that the critical role of FTO in the progression of bladder cancer and could provide a novel avenue to regulate oncogene STAT3.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.