ArticleJournal of nanobiotechnology2025
Inhibition of METTL14 overcomes CDK4/6 inhibitor resistance driven by METTL14-m6A-E2F1-axis in ERα-positive breast cancer.
Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed.
- Effects of Isorhapontigenin on Cell Viability, Colony-Forming Efficiency, and Ferroptosis via Methyltransferase-Like 14-Mediated mMolecular carcinogenesis · 2026Article
- Carboplatin Is Associated with Changes in Components of the mACS omega · 2026Article
- The Role of NMedComm · 2026Review
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- The dual regulatory role of METTL14-mediated mFrontiers in oncology · 2026Review
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Dynamic modifications of circular RNAs drive oncogenesis.Epigenomics · 2025Review
- CRISPR screening approaches in breast cancer research.Cancer metastasis reviews · 2025Review
- Integrative analysis of m6A-SNPs and single-cell RNA sequencing reveals key drivers of endocrine combined with CDK4/6 inhibitor therapy resistance in ER+ breast cancer.Frontiers in pharmacology · 2025Article
- Small-molecule and peptide inhibitors of m6A regulators.Frontiers in oncology · 2025Review
- METTL14 in tumor immunity: epitranscriptomic regulation and therapeutic potential.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
CDK4/6i, the first-line drug for treating ERα-positive breast cancer, significantly improves clinical outcomes. However, CDK4/6i resistance often develops and remains a major hurdle, and the underlying mechanisms remain challenging to fully investigate. Here, we used Genome-wide CRISPR/Cas9 library screening combined with single-cell sequencing to screen for molecules mediating CDK4/6i resistance and identified METTL14 as a determinant of CDK4/6i sensitivity. Clinical samples and datasets were analyzed and in vitro and in vivo experiments were performed to confirm the critical function of METTL14 in CDK4/6i resistance. Mechanistically, METTL14 can induce an increase in E2F1 expression in breast cancer cells via an m6A IGF2BP2-dependent mechanism and thus promote CDK4/6i resistance. Furthermore, through a small molecule screen, a novel METTL14 inhibitor named WKYMVM, which can restore sensitivity to CDK4/6i in CDK4/6i-resistant breast cancer cells, was identified. Treatment with folate-conjugated liposomes targeting breast cancer cells that contained both a CDK4/6i and WKYMVM revealed the synergistic effect of METTL14 inhibition with CDK4/6i therapy in a CDK4/6i-resistant PDX model. Together, our findings reveal the mechanism of CDK4/6i resistance and provide a strategy for overcoming CDK4/6i resistance via METTL14 inhibition.
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