ArticleBioengineered2022
The potential role of methyltransferase-like 5 in deficient mismatch repair of uterine corpus endometrial carcinoma.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Targeting the METTL5-MGST1 axis for cancer therapy: molecular mechanisms and therapeutic implications.Molecular biology reports · 2026Review
- METTL5-mediated m6A modification of 18S rRNA drives oral squamous cell carcinoma progression by enhancing CCND3 translation.Oncology letters · 2026Article
- METTL4 and METTL5 as biomarkers for recurrence-free survival in hepatocellular carcinoma patients.Future oncology (London, England) · 2025Article
- METTL protein family: focusing on the occurrence, progression and treatment of cancer.Biomarker research · 2024Review
- Article
- METTL5 promotes gastric cancer progressionWorld journal of gastrointestinal oncology · 2024Article
- Targeting RNA modifications with pharmacological agents: New frontiers in cancer therapy.Cancer medicine · 2024Review
- Exploring the role of PRDX4 in the development of uterine corpus endometrial carcinoma.Medical oncology (Northwood, London, England) · 2024Article
- METTL5-mediated 18S rRNA mMolecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- METTL5 serves as a diagnostic and prognostic biomarker in hepatocellular carcinoma by influencing the immune microenvironment.Scientific reports · 2023Article
- METTLing in Stem Cell and Cancer Biology.Stem cell reviews and reports · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To explore the potential function of methyltransferase-like 5 (METTL5) in uterine corpus endometrial carcinoma (UCEC) and verify the relationship between deficient DNA mismatch repair (MMR) and METTL5. We used bioinformatics to predict the possible role of METTL5 and molecular biology methods to analyze METTL5 expression. We observed UCEC proliferation, development, and apoptosis using a METTL5 knockdown lentivirus and, coupled with METTL5 bioinformatics and Western blot analysis, detected microsatellite instability (MSI) and MMR. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed. Finally, some METTL5-associated gene mutations in UCECs were detected. Results show that METTL5 expression in UCEC tumor tissue was increased, and UCEC patients with high METTL5 expression had worse prognostic outcomes. We also observed the highest METTL5 expression level in KLE cells. Furthermore, knocking down METTL5 weakened the proliferation, reduced tumor volume and biomarkers, and increased apoptosis. Moreover, METTL5 knockdown induced the MSH2, MSH6 and PMS2 expression in MMR. METTL5 was negatively correlated with gene silencing, mRNA binding, olfactory receptor activity, antigen processing and presentation, cytosolic DNA sensing, olfactory transduction, and RIG-1-like and Toll-like receptor signaling pathways. METTL5 may regulate MMR protein levels in UCECs, thus enhancing UCEC proliferation, development, and prognosis.
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