ArticleProceedings of the National Academy of Sciences of the United States of America2025
Activation of epigenetic reprogramming via crotonylation overcomes resistance to EGFR-TKI therapy in lung cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- SUMOylation activates ECHS1 for adaptive catabolism in lung cancer.Cell death & disease · 2026Article
- Multidrug resistance in cancer: current understandings and future perspective.Molecular biomedicine · 2026Review
- Simvastatin Restores Cisplatin Sensitivity by Suppressing the Caveolin-1-Mediated PI3K/AKT Signaling Pathway in Cisplatin-Resistant Cervical Cancer Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Coming to light: the transcriptional regulatory roles of histone lysine crotonylation in health and disease.Cellular & molecular biology letters · 2026Review
- Targeting a super-enhancer induced aldehyde dehydrogenase metabolic loop mitigates CDK4/6 inhibitor resistance in estrogen receptor-positive cancers.Nature communications · 2026Article
- FN-1501 Synergistically Enhances Almonertinib Efficacy in EGFR-TKI-Resistant Lung Adenocarcinoma through Ferroptosis Induction.Anti-cancer agents in medicinal chemistry · 2026Article
- Drug resistance in cancer: molecular mechanisms and emerging treatment strategies.Molecular biomedicine · 2025Review
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18 authors.
Funding
Abstract
Posttranslational modifications (PTMs) on histones play critical roles in cellular processes, including gene expression and tumorigenesis. However, the regulatory mechanisms and functional consequences of newly identified lysine acylation modifications in cancer therapy remain to be elucidated. Here, we established diverse preclinical tumor models resistant to epithelial growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) and focused on histone lysine crotonylation (Kcr), as it exhibited more pronounced alterations compared to other acylations. Next, we identified acyl-CoA synthetase short-chain family member 2 as a key regulator responsible for the resistance-associated decrease in crotonylation levels. Furthermore, integrated crotonylomic, transcriptomic, and epigenomic profiling, supplemented by gene manipulation studies, revealed that EGFR-TKI resistance resulted from transcriptional suppression of
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