ArticleOncogene2026
An H4K12la/CEBPB-AKR1C2 signaling axis modulates the mTOR pathway to regulate cisplatin resistance in lung cancer.
Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- The crosstalk between RNA m6A modification and protein lactylation: emerging insights into tumor progression.Oncogene · 2026Review
- Natural Plant Bioactives as Regulators of Histone Modifications: Bridging Epigenetics and Anticancer Therapy.Phytotherapy research : PTR · 2026Review
- Histone H3K18 lactylation promotes malignancy progression in non-small cell lung cancer through TCN1 upregulation.Journal of molecular histology · 2026Article
- Analysis of Metabolic Differences and Core Regulatory Pathways in Lactic Acid Bacteria-Fermented Broths of DifferentFoods (Basel, Switzerland) · 2026Article
- [Research Progress on Glycolytic Reprogramming and Lactylation Crosstalk in Tumors].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Review
- Glycolysis-mediated H3K18la modifications drive aggressive bladder cancer through metabolic and epigenetic reprogramming.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Histone lactylation, a recently discovered epigenetic modification, has been shown to play a critical role in regulating gene expression and cellular functions. However, its involvement in cisplatin (CDDP) resistance in non-small cell lung cancer (NSCLC) remains poorly understood. In this study, we demonstrated that histone lactylation is closely associated with CDDP resistance and correlates with poor prognosis of NSCLC. Mechanistically, H4K12la (histone e 4 lysine 12 lactylation) levels and CEBPB (CCAAT/enhancer-binding protein beta) had a cooperative effect on the regulation of AKR1C2 (Aldo-Keto reductase 1C2). Furthermore, AKR1C2 knockdown activates the mTOR oncogenic signaling pathway. Importantly, genetic manipulation of AKR1C2 or the combination of CDDP with an mTOR inhibitor effectively reverse CDDP resistance in NSCLC/CDDP cells. These findings highlighted the potential of AKR1C2 as a predictive biomarker for patient response to CDDP therapy. Additionally, our study established a novel link between histone lactylation and CDDP resistance, providing new insights into the epigenetic regulation in NSCLC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.