ArticleResearch (Washington, D.C.)2024
The FTO Mediated N6-Methyladenosine Modification of DDIT4 Regulation with Tumorigenesis and Metastasis in Prostate Cancer.
Article in Research (Washington, D.C.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 24 citations in OpenAlex.
- The role, regulatory mechanisms, and therapeutic implications of FTO in gastrointestinal cancer.Genes & diseases · 2026Review
- FTO in Bone Diseases: Functions, Mechanisms and Therapeutic Potential.Biomolecules · 2026Review
- The Role of NMedComm · 2026Review
- ZFP36L1 Enhances Microglial Ferroptosis in Ischemic Stroke by Reducing FTO-Mediated N6-Methyladenosine Demethylation of ACSL1 mRNA.The Kaohsiung journal of medical sciences · 2026Article
- Transcriptional and epigenetic reprogramming, lineage plasticity and therapy resistance in prostate cancer.Journal of the National Cancer Center · 2026Review
- RNA methylation in urological cancers: regulatory logic, biological functions, and clinical relevance.Frontiers in immunology · 2026Review
- Epitranscriptomic control of epithelial-mesenchymal transition in cancer: mechanisms, plasticity, and therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Reader-dependent functional duality of FTO: a context-switching node at the intersection of immune evasion and therapeutic resistance.Frontiers in immunology · 2026Review
- Obesity-linked genes may promote prostate cancer among Asian and Hispanic immigrants to North America.Frontiers in public health · 2026Review
- The emerging role of mFrontiers in immunology · 2026Review
- CBX8 suppresses autophagy-dependent senescence in colorectal cancer by modulating the mTOR signaling pathway.International journal of biological sciences · 2026Article
- Nidogen 1-enriched extracellular vesicles promote liver metastasis by inducing EMT and activating stellate cells.iScience · 2025Article
- The Central Role of m6A as Epigenetic Regulator in Metabolic Disorders of Therapeutic Potential and Clinical Implications.Molecular neurobiology · 2025Review
- METTL14-mediated mEpigenetics · 2025Article
- MJournal of ovarian research · 2025Article
- Unveiling prognostic biomarkers and immunotherapeutic insights in prostate cancer through multi-omics and machine learning.European journal of medical research · 2025Article
- Hypoxia-mediated mJournal of translational medicine · 2025Review
- Increased susceptibility to prostate cancer biomarkers in the offspring of male mouse progenitors with lifelong or early life exposure to high-fat diet.European journal of nutrition · 2025Article
- Biological roles of enhancer RNA m6A modification and its implications in cancer.Cell communication and signaling : CCS · 2025Review
- Analysis of Genotype and Expression of FTO and ALKBH5 in a MENA-Region Renal Cell Carcinoma Cohort.Cancers · 2025Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The progression of numerous malignancies has been linked to N6-methyladenosine (m6A) alteration. However, the opposite trend of m6A levels in the development and metastasis of cancer has not been reported. This study aimed to evaluate the biological function and mechanism of fat mass and obesity-associated protein (FTO) in regulating m6A modification in prostate cancer development and epithelial-mesenchymal transition (EMT). An EMT model of LNCaP and PC-3 cells was established with transforming growth factor-β treatment, and FTO knockout cell line was established in prostate cancer cells using the CRISPR/Cas9 gene editing technology. The level of m6A modification in tumor tissues was higher than that in normal prostate tissues; m6A levels were decreased after EMT. FTO deletion increased m6A expression and enhanced PC-3 cell motility, invasion, and EMT both in vitro and in vivo. RNA sequencing and functional investigations suggested that DDIT4, a novel EMT target gene, plays a role in m6A-regulated EMT, which was recognized and stabilized by the m6A effector IGF2BP2/3. Decreased FTO expression was an independent indicator of worse survival, and the level of DDIT4 was considerably elevated in patients with bone metastasis. Thus, this study revealed that the m6A demethylase FTO can play different roles in prostate cancer as a regulator of EMT and an inhibitor of m6A modification. Moreover, DDIT4 can be suggested as a possible biomarker for prostate cancer metastasis prediction.
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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.