ArticleInternational journal of biological sciences2024
METTL16 suppressed the proliferation and cisplatin-chemoresistance of bladder cancer by degrading PMEPA1 mRNA in a m6A manner through autophagy pathway.
Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 32 citations in OpenAlex.
- Demethylase FTO attenuates atherosclerotic plaque via upregulating ABCA1 and ABCG1 expression by targeting ATG5.Molecular medicine reports · 2026Article
- METTL16 promotes colorectal cancer progression and CD8Medical oncology (Northwood, London, England) · 2026Article
- m6A-Driven Pexophagy Triggers Placental Ferroptosis to Impair Fetal Growth Upon Environmental Stress.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- N6-Methyladenosine RNA Methylation: A Key Regulator in Male Reproductive Disorders and Urological Cancers.The world journal of men's health · 2026Review
- RNA methylation in cell death: mechanisms and clinical applications.Molecular cancer · 2026Review
- Abnormal Sialylation Promotes Chemotherapy Resistance in Bladder Cancer via the PI3K-AKT-mTOR Signaling Pathway.Cancers · 2026Article
- METTL16 in cancer: Roles and regulatory mechanisms.Genes & diseases · 2026Review
- Review
- METTL16 promotes PD-L1 expression and mediates immunosuppression in B-cell lymphomas via mAmerican journal of translational research · 2026Article
- Loss of UFL1 confers enzalutamide resistance of prostate tumors by regulating METTL16-mediated m6A modification of EEF1A1 mRNA.International journal of biological sciences · 2026Article
- The Quartet of Core Oncogenic Drivers in Neuroendocrine Prostate Cancer: Multi-Omics Dataset Integration to Forge a Translational Link Between Biology and Precision Therapy.International journal of biological sciences · 2026Review
- Hypoxia-triggered autophagy modulates cisplatin resistance in non-small cell lung Cancer via EIF2AK3-dependent PI3K/AKT signaling and mTOR-independent mechanisms.Cell death discovery · 2025Article
- The Central Role of m6A as Epigenetic Regulator in Metabolic Disorders of Therapeutic Potential and Clinical Implications.Molecular neurobiology · 2025Review
- BoltzGen: Toward Universal Binder Design.bioRxiv : the preprint server for biology · 2025Article
- Repurposing Antimalarials for Oral Cancer: Selective Efficacy of Hydroxychloroquine on Gingival Squamous Cell Carcinoma.International journal of molecular sciences · 2025Article
- The methyltransferase-like proteins as core regulators of nucleic acid modifications and post-translation modification of proteins in disease pathogenesis and therapeutic implications.Biomarker research · 2025Review
- Targeting METTL16 attenuates mesangial cell viability and fibrosis in a high-glucose state by suppressing m6A modification and the expression of RAP1B.BMC molecular and cell biology · 2025Article
- Platycodin D-mediated METTL16 downregulation promotes docetaxel treatment of prostate cancer by regulating ferroptosis.BMC cancer · 2025Article
- RNA mCell investigation · 2025Article
- NAP1L1 degradation by FBXW7 reduces the deubiquitination of HDGF-p62 signaling to stimulate autophagy and induce primary cisplatin chemosensitivity in nasopharyngeal carcinoma.Molecular cancer · 2025Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N6-methyladenosine (m6A) is important in the physiological processes of many species. Methyltransferase-like 16 (METTL16) is a novel discovered m6A methylase, regulating various tumors in an m6A-dependent manner. However, its function in bladder cancer (BLCA) remains largely unclear. In the present study, we found that low expression of METTL16 predicted poor survival in BLCA patients. METTL16 inhibited the proliferation and cisplatin-resistance function of bladder cancer cells
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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.