ArticleClinical epigenetics2021
METTL3-dependent MALAT1 delocalization drives c-Myc induction in thymic epithelial tumors.
Article in Clinical epigenetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 34 citations in OpenAlex.
- PRRC2A-mediated mCell death & disease · 2026Article
- The lncRNA-m6A axis in cancer: a bidirectional regulatory network in tumor progression and therapeutic resistance.Journal of translational medicine · 2026Review
- mFrontiers in cell and developmental biology · 2026Review
- RBM15 Enhances 5-Fluorouracil Drug Sensitivity and Suppresses Gastric Cancer Progression by Modulating N6-Methyladenosine Modification of ECT2-Dependent IGF2BP3.Research (Washington, D.C.) · 2026Article
- Deregulation and delocalization of the mHistology and histopathology · 2025Article
- METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025Review
- Glutamine metabolism and ammonia death: targeted modulation for enhanced cancer immunotherapy.Frontiers in immunology · 2025Review
- The role of N(6)-methyladenosine (m6a) modification in cancer: recent advances and future directions.EXCLI journal · 2025Review
- Linking ferroptosis to thymic involution.Nature aging · 2024Article
- Non-Mutational Key Features in the Biology of Thymomas.Cancers · 2024Review
- Multi-omics sequencing revealed endostar combined with cisplatin treated non small cell lung cancer via anti-angiogenesis.BMC cancer · 2024Article
- Methyltransferase-like 14 promotes the tumorigenesis and proliferation of pancreatic cancer cells through myc proto-oncogene signaling pathway.CytoJournal · 2024Article
- The indispensability of methyltransferase-like 3 in the immune system: from maintaining homeostasis to driving function.Frontiers in immunology · 2024Review
- Methyltransferase-like proteins in cancer biology and potential therapeutic targeting.Journal of hematology & oncology · 2023Review
- Novel insights into mutual regulation between NCancer cell international · 2023Review
- Novel insights into the multifaceted roles of mBiomarker research · 2023Review
- The roles of N6-methyladenosine and its target regulatory noncoding RNAs in tumors: classification, mechanisms, and potential therapeutic implications.Experimental & molecular medicine · 2023Review
- Epigenetics of Thymic Epithelial Tumors.Cancers · 2023Review
- Unraveling molecular networks in thymic epithelial tumors: deciphering the unique signatures.Frontiers in immunology · 2023Review
- Crosstalk between mOncogene · 2022Review
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Authors and funding
22 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundThymic epithelial tumors (TETs) are rare neoplasms, originating from epithelial thymic cells. The oncogenic potential of these rare neoplasms is still largely undefined, and a deeper molecular characterization could result in a relevant advance in their management, greatly improving diagnosis, prognosis and treatment choice. Deregulation of N6-methyladenosine (m
resultsIn this study, we characterized that METTL3 contributes to Thymic Epithelial Tumor phenotype. We evidenced that METTL3 is overexpressed in tumor tissue compared to normal counterpart. Silencing of METTL3 expression in thymic carcinoma cells results in reduced cell proliferation and overall translation rate. Of note, METTL3 is responsible for the induction of c-MYC expression in TET cells. Specifically, high expression of c-MYC protein is enabled by lncRNA MALAT1, which is methylated and delocalized by METTL3. Interestingly, blocking of c-MYC by using JQ1 inhibitor cooperates with METTL3 depletion in the inhibition of proliferation and induction of cell death.
conclusionThis study highlighted METTL3 as a tumor promoter in Thymic tumors and c-MYC as a promising target to be exploited for the treatment of TET.
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