ArticleCell & bioscience2022
m6A demethylase FTO promotes tumor progression via regulation of lipid metabolism in esophageal cancer.
Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 50 citations in OpenAlex.
- Long noncoding RNA PCAT7 confers radioresistance of esophageal squamous cell carcinoma by promoting GCLM-mediated anti-ferroptosis.Journal of translational medicine · 2026Article
- RNA Methylation in Cancer Metabolism: from Mechanisms to Therapeutic Opportunities.International journal of biological sciences · 2026Review
- Development and validation of an m6A and autophagy related lncRNAs signature for predicting survival and modulating the immune microenvironment in esophageal squamous cell carcinoma.Frontiers in immunology · 2026Article
- ACSL4 as a context-dependent metabolic switch in hepatocellular carcinoma: implications for ferroptosis and immunotherapy.Frontiers in immunology · 2026Review
- FTO-mediated m6A demethylation of BECN1 mRNA promotes hepatic steatosis by impairing autophagy.BMC immunology · 2025Article
- Unveiling the role of m6A modification in esophageal cancer: a new frontier in tumor innate interferon immunity.Cancer cell international · 2025Review
- RNA methylation in hepatocellular carcinoma: from metabolic reprogramming and immune escape mechanisms to small molecule inhibitor development.Journal of translational medicine · 2025Review
- Article
- Repurposing FDA-approved drugs to find a novel inhibitor of alpha-ketoglutarate-dependent dioxygenase FTO to treat esophageal cancer.Research in pharmaceutical sciences · 2025Article
- Aberrant overexpression of m6A writer and reader genes in pediatric B-Cell Acute Lymphoblastic Leukemia (B-ALL).Translational oncology · 2025Article
- Epitranscriptomic Role of m6A in Obesity-Associated Disorders and Cancer Metabolic Reprogramming.Genes · 2025Review
- Role and mechanisms of m6A demethylases in digestive system tumors.American journal of cancer research · 2025Review
- RNA Binding Motif Protein 15 (RBM15): Structure, Function and Its Research Progress in Tumors.International journal of general medicine · 2025Review
- Regulatory mechanisms of m6A RNA methylation in esophageal cancer: a comprehensive review.Frontiers in genetics · 2025Review
- RNA modifications in cancer.MedComm · 2025Review
- High expression of RBM15 is associated with better prognosis in esophageal squamous cell carcinoma.Journal of gastrointestinal oncology · 2024Article
- Role of N6-methyladenosine methylation in nasopharyngeal carcinoma: current insights and future prospective.Cell death discovery · 2024Review
- Characterization and validation of a prognostic model for the N6-methyladenosine-associated ferroptosis gene in colon adenocarcinoma.Translational cancer research · 2024Article
- Progression of mCell death discovery · 2024Review
- Insights into the role of RNA mGenes & diseases · 2024Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundEpitranscriptomics studies have contributed greatly to the development of research on human cancers. In recent years, N6-methyladenosine (m6A), an RNA modification on the N-6 position of adenosine, has been found to play a potential role in epigenetic regulation. Therefore, we aimed to evaluate the regulation of cancer progression properties by m6A.
resultsWe found that m6A demethylase fat mass and obesity-associated protein (FTO) was highly expressed in esophageal cancer (EC) stem-like cells, and that its level was also substantially increased in EC tissues, which was closely correlated with a poor prognosis in EC patients. FTO knockdown significantly inhibited the proliferation, invasion, stemness, and tumorigenicity of EC cells, whereas FTO overexpression promoted these characteristics. Furthermore, integrated transcriptome and meRIP-seq analyses revealed that HSD17B11 may be a target gene regulated by FTO. Moreover, FTO promoted the formation of lipid droplets in EC cells by enhancing HSD17B11 expression. Furthermore, depleting YTHDF1 increased the protein level of HSD17B11.
conclusionsThese data indicate that FTO may rely on the reading protein YTHDF1 to affect the translation pathway of the HSD17B11 gene to regulate the formation of lipid droplets in EC cells, thereby promoting the development of EC. The understanding of the role of epitranscriptomics in the development of EC will lay a theoretical foundation for seeking new anticancer therapies.
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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 OpenQuestion graph.