ArticleCancer management and research2019
miR-600 inhibits lung cancer via downregulating the expression of METTL3.
Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.
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Who cites it
100 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Prognostic Roles of N6-Methyladenosine METTL3 in Different Cancers: A System Review and Meta-Analysis.Cancer control : journal of the Moffitt Cancer CenterPooled it
- Exercise, Demethylase FTO, Neurological Disorders, and Neuropathic Pain: Potential Molecular Mechanisms.CNS neuroscience & therapeutics · 2026Review
- Ligand-Induced Opening of a Cryptic Pocket in METTL14.ACS bio & med chem Au · 2026Article
- METTL3-mediated m6A modification of FDX1 confers resistance to cuproptosis and promotes hepatocellular carcinoma progression.Communications biology · 2026Article
- The mFrontiers in cell and developmental biology · 2026Review
- Pyroptosis Regulated by N6-Methyladenosine Modification: Implications for Pyroptosis-Related Disease Therapy.Journal of innate immunity · 2026Review
- MiR-4701-3p predicts prognosis of non-small cell lung cancer and regulates cell biological behaviors.Hereditas · 2025Article
- Non-coding RNAs and regulation of the PI3K signaling pathway in lung cancer: Recent insights and potential clinical applications.Non-coding RNA research · 2025Review
- The impact of METTL3 on bladder cancer through mFrontiers in oncology · 2025Review
- The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024Review
- Multimodal tumor suppression by METTL3 gene knockdown in melanoma and colon cancer cells.Histochemistry and cell biology · 2024Article
- Crosstalk between RNA mPlant communications · 2024Review
- The roles of non-coding RNAs in Hirschsprung's disease.Non-coding RNA research · 2024Review
- Ferroptosis: a critical mechanism of NScience China. Life sciences · 2024Review
- Association between methyltransferase-like 3 and non-small cell lung cancer: pathogenesis, therapeutic resistance, and clinical applications.Translational lung cancer research · 2024Review
- Article
- Non-coding RNA-Mediated N6-Methyladenosine (mNon-coding RNA research · 2024Review
- METTL3 Mediates Microglial Activation and Blood-Brain Barrier Permeability in Cerebral Ischemic Stroke by Regulating NLRP3 Inflammasomes Through m6A Methylation Modification.Neurotoxicity research · 2024Article
- The role of the methyltransferase METTL3 in prostate cancer: a potential therapeutic target.BMC cancer · 2024Review
- The role of CEMIP in cancers and its transcriptional and post-transcriptional regulation.PeerJ · 2024Review
40 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMethyltransferase like 3 (METTL3) is an RNA methyltransferase implicated in mRNA biogenesis, decay, and translation control through N
methodsTo find new treatment strategies for lung cancer and to elucidate the mechanism underlying the phenomenon, we treated the human lung cancer cell lines A549 and H1299 to investigate the effect of METTL3 on lung cancer.
resultsWe observed that knockdown of METTL3 inhibited the survival and proliferation of A549 and H1299 cells. The migration and proliferation of both cell lines were significantly decreased, and the apoptosis was induced in comparison with control cells. These results were further confirmed by the transfection of miRNA of METTL3 increased the Bax/Bcl-2 ratio in A549 and H1299 cells, which is a sign that mitochondrial apoptotic pathway was triggered. The PI3K/Akt pathway is implicated in cell growth and survival and we also observed that knockdown of METTL3 changed the expression and phosphorylation of proteins of PI3K signaling pathway members. Further, our results demonstrated that miR-600 inhibited the expression of METTL3 and reversed the positive effect of METTL3 on NSCLC progression, indicating an miR-600/METTL3 pathway in NSCLC.
conclusionThese data suggested that miR-600 inhibited lung cancer via down-regulating METTL3 expression, and knockdown of METTL3 might be used as a novel strategy for lung cancer therapy.
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