ArticleJournal of experimental & clinical cancer research : CR2025
Lactylation-driven KRT19 promotes non-small cell lung cancer progression by suppressing cellular senescence.
Article in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- The crosstalk between RNA m6A modification and protein lactylation: emerging insights into tumor progression.Oncogene · 2026Review
- Crosstalk between lactylation and other post-translational modifications in health and diseases.Molecular biomedicine · 2026Review
- The metabolic-epigenetic landscape of aging: interplay between histone acetylation, lactylation, and glycation.Frontiers in aging · 2026Review
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Authors and funding
11 authors.
Funding
Abstract
backgroundCellular senescence provides a protective barrier against tumorigenesis. However, the detailed mechanisms underlying tumor cells bypass senescence to malignant progression of non-small cell lung cancer (NSCLC) are still poorly understood.
methodsIn this study, we assessed the impact of KRT19 on NSCLC using xenograft tumor models, EdU, CCK8, colony formation and transwell assay. We performed chromatin immunoprecipitation sequencing and dual luciferase reporter assay to explore the mechanism through which H3K18 lactylation (H3K18la) mediated KRT19. The mechanism underlying KRT19 regulated p21-driven cellular senescence was explored by senescence-associated β-galactosidase staining, flow cytometry and further identified by RNA sequencing, mass spectrometry, immunofluorescence, co-immunoprecipitation and protein ubiquitination assay. The clinical significance of H3K18la/KRT19/p21 was determined by immunohistochemistry in human NSCLC specimens and bioinformatics analysis of TCGA database and Kaplan-Meier method. We evaluated the effects of KRT19 inhibition and anti-PD-1 on NSCLC growth and immune infiltration using xenograft tumor models, flow cytometry and CIBERSORT.
resultsOur study revealed that elevated expression of KRT19 was correlated with poor prognosis of NSCLC patients and exhibited oncogenic activity in NSCLC. Mechanistically, lactate-derived H3K18la activated the transcription of KRT19 via directly binding to its promoter. KRT19 blocked the transcriptional activation of p21 by p53, alternatively, KRT19 also interacted with MYH9 to facilitate ubiquitination of p21 at K16. More significantly, blockade of KRT19 potently enhanced the cytotoxic function of tumor-infiltrating CD8
conclusionOur study emphasizes the importance of lactylation-driven KRT19 for overriding senescence and promoting NSCLC progression, reinforcing the potential of combination therapy strategies with KRT19 inhibitors to yield favorable responses in patients with NSCLC.
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