ArticleBiology direct2025
Methyltransferase-like 7B participates in bladder cancer via ACSL3 m
Article in Biology direct, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- N6-Methyladenosine RNA Methylation: A Key Regulator in Male Reproductive Disorders and Urological Cancers.The world journal of men's health · 2026Review
- [Methyltransferase-like protein 7B promotes glycolysis and malignant progression in papillary thyroid carcinoma cells via the USP28/HIF-1α axis].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Article
- Degradation of ACSL3 by influenza A virus shifts unfolded protein response from antiviral defense to viral evasion.Virologica Sinica · 2026Article
- RNA modifications and cancer ferroptosis.Cancer cell international · 2026Review
- The multifaceted roles of the ACSL family in cancer: Metabolic reprogramming, ferroptosis regulation and tumour immune microenvironment remodelling.Clinical and translational medicine · 2026Review
- Ferroptosis-autophagy crosstalk in bladder cancer: mechanisms and therapeutic implications.Molecular cancer · 2026Review
- RNA m6A modification-regulated ferroptosis in cancer: mechanism and therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- 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
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundBladder cancer (BC) is a malignant tumor. Methyltransferase-like 7B (MEETL7B) is a methyltransferase and its role in BC has not yet been revealed.
methodStable METTL7B knockdown or overexpression were achieved by lentiviral transduction in SW780 and TCCSUP cell lines. Xenografts tumors were established via subcutaneous injection of stable transfectants in BALB/c mice.
resultsA database search indicated that METTL7B was elevated in BC and it was validated in BC cell lines. METTL7B silencing suppressed cell proliferation and tumorigenesis in vitro and in vivo. Besides, METTL7B knockdown induced cell cycle arrest in G1 phase with a reduction in cyclin D1(CCND1), CDK4, and CDK6 levels and an elevation in CDKN2D levels in cells. Considering that ferroptosis is emerging as a therapeutic target for cancer, and the possible relationship between METTL7B and antioxidant enzymes. We, here, examined that ectopic METTL7B expression abolished ferroptosis markers in cells raised by Erastin treatment, including the production of lipid ROS, the increased cellular iron and MDA content, the decreased gene expression of ACSL3, FANCD2, and FADS2, as well as the mitochondrial injury observed by electron microscopy. Mechanically, ectopic METTL7B expression promoted m
conclusionsMETTL7B is involved in BC development and progression. METTL7B may mediate m
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