ArticleJournal of immunology research2021
METTL3 Intensifies the Progress of Oral Squamous Cell Carcinoma via Modulating the m6A Amount of PRMT5 and PD-L1.
Article in Journal of immunology research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed.
- METTL3‑mediated OTUB1 sustains PD‑L1 protein stability via deubiquitination and promotes immune evasion in oral squamous cell carcinoma.Molecular and cellular biochemistry · 2026Article
- Identification of METTL3 and PRMT5 as an oncogenic pair for the prognosis and therapeutic targets of colorectal cancer subtype.Clinical epigenetics · 2026Article
- PRMT5 encourages cell migration and metastasis of tongue squamous cell carcinoma through methylating ΔNp63α.Cell death and differentiation · 2026Article
- Therapy-induced mRNA, rRNA and tRNA methylation alterations confer tolerance phenotype in tumor cells: mechanism and implications.International journal of biological sciences · 2026Review
- KIAA1429 impairs anti-tumor immunity via regulation of PD-L1 and CD8Scientific reports · 2025Article
- Post-translational modifications in the oral microenvironment: Stem cell regulation from periodontal regeneration to oral cancer therapy.World journal of stem cells · 2025Review
- Arginine methylation in cancer: mechanisms and therapeutic implications.Biomarker research · 2025Review
- Deciphering the role of IGF2BP2 and PRMT5 in gallbladder cancer progression: insights from multi-omics analysis.British journal of cancer · 2025Article
- Article
- Abnormal changes in metabolites caused by mJournal of advanced research · 2025Review
- The Role of MClinical reviews in allergy & immunology · 2025Review
- N6-methyladenosine RNA modification in head and neck squamous cell carcinoma (HNSCC): current status and future insights.Medical oncology (Northwood, London, England) · 2024Review
- METTL protein family: focusing on the occurrence, progression and treatment of cancer.Biomarker research · 2024Review
- Mechanism of apoptosis in oral squamous cell carcinoma promoted by cardamonin through PI3K/AKT signaling pathway.Scientific reports · 2024Article
- Long noncoding RNA MALAT-1: A versatile regulator in cancer progression, metastasis, immunity, and therapeutic resistance.Non-coding RNA research · 2024Review
- Ferroptosis: a critical mechanism of NScience China. Life sciences · 2024Review
- Small molecule inhibitors targeting mJournal of hematology & oncology · 2024Review
- Harnessing m1A modification: a new frontier in cancer immunotherapy.Frontiers in immunology · 2024Review
- The role of m6A epigenetic modifications in tumor coding and non-coding RNA processing.Cell communication and signaling : CCS · 2023Review
- RCN1 deficiency inhibits oral squamous cell carcinoma progression and THP-1 macrophage M2 polarization.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N6-Methyladenosine (m6A) modification is one of the commonest chemical modifications in eukaryotic mRNAs, which has essential effects on mRNA translation, splicing, and stability. Currently, there is a rising concern on the regulatory role of m6A in tumorigenesis. As a known component in the m6A methyltransferase complex, METTL3 (methyltransferase-like 3) plays an essential role in m6A methylation. Till now, the functions of METTL3 in oral squamous cell carcinoma (OSCC) and its relative mechanism remain to be explored. In this research, through the GEPIA database, we found that high METTL3 expression has a correlation with poor prognosis of squamous cell carcinoma of head and neck. qRT-PCR displayed that METTL3 was highly expressed in OSCC cells. Functionally, METTL3 knockdown reduced the invasion, migration, and proliferation competence of OSCC cells and attenuated the activation of CD8+ T cells. In contrast, METTL3 overexpression resulted in opposite results. GEPIA, UALCAN, and SRAMP databases, PCR, western blot, and m6A RNA methylation assay confirmed the m6A modification of PRMT5 and PD-L1 mediated by METTL3. In conclusion, our results displayed that METTL3 intensified the metastasis and proliferation of OSCC by modulating the m6A amounts of PRMT5 and PD-L1, suggesting that METTL3 may be a therapeutic target for OSCC patients.
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