ArticleMolecular cancer2022
Methyltransferase like 7B is a potential therapeutic target for reversing EGFR-TKIs resistance in lung adenocarcinoma.
Article in Molecular cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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61 citing papers in PubMed, 84 citations in OpenAlex.
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- Methyltransferase-like 7B promotes M2-like macrophage polarization in lung adenocarcinoma via upregulating human epidermal growth factor receptor 3 expression and secretion.Oncology letters · 2026Article
- DYT8 drives lung adenocarcinoma through EGFR-mediated PSMC6 recruitment and uncharacterized phosphorylation at Ser 306 and 525 of c-Src.Acta pharmacologica Sinica · 2026Article
- Clinical Efficacy of Tislelizumab Plus Gemcitabine-Nab-Paclitaxel for Borderline Resectable Pancreatic Cancer and Chemoresistance Analysis: A Prospective Pilot Study.Annals of surgical oncology · 2026Article
- METTL7B Expression in Sepsis: Association With Disease Severity and 28-Day Mortality.Journal of clinical laboratory analysis · 2026Article
- METTL7B attenuates pathological cardiac hypertrophy via m6A-associated regulation of HK3.Molecular and cellular biochemistry · 2026Article
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- LPIN2 contributes to tyrosine kinase inhibitor resistance via activation of PI3K pathway.Translational lung cancer research · 2026Article
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- Update of the Methyltransferase Gene Family: Classification, Evolution and Biological Functions.Human genomics · 2026Review
- Inhibition of the RORC/GPX4 mediated ferroptosis regulatory axis suppresses tumor growth and alleviates enzalutamide resistance in prostate cancer.Cellular & molecular biology letters · 2026Article
- The role of m6A modification in non-small cell lung cancer: functional insights and impact on therapy resistance.Cancer cell international · 2025Review
- Mitochondria at the intersections of RNA modifications and metabolism reprogramming implications in cell death, tumor microenvironment, and immunotherapy.Journal of hematology & oncology · 2025Review
- The N6-methyladenosine-mediated cLMNB1 degrades FGFR4 to overcome osimertinib resistance in non-small cell lung cancer.Cell death & disease · 2025Article
- The methyltransferase-like proteins as core regulators of nucleic acid modifications and post-translation modification of proteins in disease pathogenesis and therapeutic implications.Biomarker research · 2025Review
- Activation of epigenetic reprogramming via crotonylation overcomes resistance to EGFR-TKI therapy in lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- C1orf116 inhibits acquired resistance to EGFR inhibitors in EGFR mutant lung adenocarcinoma by suppressing the ATM/ATR pathways.Translational lung cancer research · 2025Article
- RBM15-mediated m6A modification of XPR1 promotes the malignant progression of lung adenocarcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIdentification of potential novel targets for reversing resistance to Epidermal Growth Factor Receptor (EGFR)-tyrosine kinase inhibitors (EGFR-TKIs) holds great promise for the treatment of relapsed lung adenocarcinoma (LUAD). In the present study, we aim to investigate the role of methyltransferase-like 7B (METTL7B) in inducing EGFR-TKIs resistance in LUAD and whether it could be a therapeutic target for reversing the resistance.
methodsMETTL7B-overexpressed LUAD cell lines, gefitinib and osimertinib-resistant Cell-Derived tumor Xenograft (CDX) and Patient-Derived tumor Xenograft (PDX) mouse models were employed to evaluate the role of METTL7B in TKIs resistance. Ultraperformance liquid chromatography-tandem mass spectrometer (UPLC-MS/MS) was used to identify the metabolites regulated by METTL7B. Methylated RNA immunoprecipitation (MeRIP)-qPCR analysis was performed to measure the N
resultsIncreased expression of METTL7B was found in TKIs-resistant LUAD cells and overexpression of METTL7B in LUAD cells induced TKIs resistance both in vitro and in vivo. Activated ROS-metabolism was identified in METTL7B-overexpressed LUAD cells, accompanied with upregulated protein level of GPX4, HMOX1 and SOD1 and their enzymatic activities. Globally elevated m
conclusionsThis study uncovered a new critical link in METTL7B, glutathione metabolism and drug resistance. Our findings demonstrated that METTL7B inhibitors could be used for reversing TKIs resistance in LUAD patients.
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