ArticleCancer discovery2024
The N6-methyladenosine Epitranscriptomic Landscape of Lung Adenocarcinoma.
Article in Cancer discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed.
- PRAME Augments K63-Linked Ubiquitination and Stabilization of METTL3 to Promote Lung Adenocarcinoma Metastasis.MedComm · 2026Article
- Reprogramming resistance in advanced lung cancer: epigenetic modulation to restore therapeutic vulnerability.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- METTL3-YTHDF1-driven mMolecular and cellular biochemistry · 2026Article
- Spatial epitranscriptomics: from Cinderella to queen.Nature methods · 2026Article
- KAT2A-IGF2BP1-CXCL2 axis in the high lactate tumor microenvironment facilitates resistance to anti-PD-1 therapy in lung adenocarcinoma by recruiting myeloid-derived suppressor cells.Cell death & disease · 2026Article
- The Role of NMedComm · 2026Review
- The lncRNA DAMER selectively guides mNature cell biology · 2026Article
- METTL3-based epitranscriptomic editing screening identifies functional mNature cancer · 2026Article
- NNature reviews. Cancer · 2026Review
- Epitranscriptomic control of cancer hallmarks: Functions, mechanisms, and therapeutics of RNA modifications.Cancer cell · 2026Review
- METTL16 promotes PD-L1 expression and mediates immunosuppression in B-cell lymphomas via mAmerican journal of translational research · 2026Article
- The role of m6A modification in non-small cell lung cancer: functional insights and impact on therapy resistance.Cancer cell international · 2025Review
- Integrating machine learning and protein-ligand interaction profiling for the discovery of METTL3 inhibitors.Scientific reports · 2025Article
- A new prognostic model for lung adenocarcinoma according propionate metabolism related genes: a comprehensive bioinformatic study.Discover oncology · 2025Article
- Machine learning-assisted multi-dimensional transcriptomic analysis of cytoskeleton-related molecules and their relationship with prognosis in hepatocellular carcinoma.Scientific reports · 2025Article
- FTO Promotes Hepatocellular Carcinoma Progression by Mediating m6A Modification of BUB1 and Targeting TGF-βR1 to Activate the TGF-β Signaling Pathway.Journal of clinical and translational hepatology · 2025Article
- Comprehensive Analysis of Aberrant m6A RNA Modifications Identifies Prognostic Biomarkers in Non-Small Cell Lung Cancer.International journal of medical sciences · 2025Article
- Integrative multi-omics reveals energy metabolism-related prognostic signatures and immunogenetic landscapes in lung adenocarcinoma.Frontiers in immunology · 2025Article
- Identification of the role of MED6 in the development and prognosis of lung adenocarcinoma based on multi-omics profiling.Journal of Cancer · 2025Article
Corrections and comments
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Authors and funding
33 authors.
Funding
Abstract
Comprehensive N6-methyladenosine (m6A) epitranscriptomic profiling of primary tumors remains largely uncharted. Here, we profiled the m6A epitranscriptome of 10 nonneoplastic lung tissues and 51 lung adenocarcinoma (LUAD) tumors, integrating the corresponding transcriptomic, proteomic, and extensive clinical annotations. We identified distinct clusters and genes that were exclusively linked to disease progression through m6A modifications. In comparison with nonneoplastic lung tissues, we identified 430 transcripts to be hypo-methylated and 222 to be hyper-methylated in tumors. Among these genes, EML4 emerged as a novel metastatic driver, displaying significant hypermethylation in tumors. m6A modification promoted the translation of EML4, leading to its widespread overexpression in primary tumors. Functionally, EML4 modulated cytoskeleton dynamics by interacting with ARPC1A, enhancing lamellipodia formation, cellular motility, local invasion, and metastasis. Clinically, high EML4 protein abundance correlated with features of metastasis. METTL3 small-molecule inhibitor markedly diminished both EML4 m6A and protein abundance and efficiently suppressed lung metastases in vivo. Significance: Our study reveals a dynamic and functional epitranscriptomic landscape in LUAD, offering a valuable resource for further research in the field. We identified EML4 hypermethylation as a key driver of tumor metastasis, highlighting a novel therapeutic strategy of targeting EML4 to prevent LUAD metastasis.
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Registered trials
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