ArticleExperimental and therapeutic medicine2020
Silencing of methyltransferase-like 3 inhibits oesophageal squamous cell carcinoma.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- METTL3, an Independent Adverse Prognostic Factor for AML, Promotes the Development of AML by Modulating the PGC-1α-MAPK Pathway and PGC-1α-Antioxidant System Axis.Cancer medicine · 2025Article
- METTL3 as a novel diagnosis and treatment biomarker and its association with glycolysis, cuproptosis and ceRNA in oesophageal carcinoma.Journal of cellular and molecular medicine · 2024Article
- The diverse role of RNA methylation in esophageal cancer.Acta biochimica et biophysica Sinica · 2023Review
- Identification of m6a-related signature genes in esophageal squamous cell carcinoma by machine learning method.Frontiers in genetics · 2023Article
- The Role of mCancers · 2022Review
- Recent advances of mCancer cell international · 2021Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methyltransferase-like 3 (METTL3) is a methyltransferase responsible for N6-methyladenosine mRNA modifications, which has been demonstrated to serve oncogenic roles in various types of cancer; however, the exact function of METTL3 in oesophageal squamous cell carcinoma (ESCC) has not been determined. The present study aimed to explore the regulatory role of METTL3 in ESCC. In the present study, reverse transcription-quantitative PCR and western blotting were used to examine mRNA and protein expression, CCK-8 assays and flow cytometry were used to determine cellular viability and apoptosis, and wound healing and Transwell assays were conducted to study cellular migration and invasion. The expression levels of METTL3 were significantly higher in ESCC tissues and cell lines compared with adjacent non-tumour tissues and the normal oesophageal epithelial cell line HET-1A, respectively. Increased METTL3 expression was associated with an advanced clinical stage of ESCC and poorer prognosis. Furthermore, the genetic knockdown of METTL3 using small interfering RNA significantly suppressed ESCC growth, invasion and migration
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