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Updated: Jan 9, 2026
Author Spotlight: Epigenetic Modifications and Metabolic Rewiring as Targets for Cancer Therapy
Published on: October 18, 2024
Histone Modification Networks Reshape the Metabolism and Treatment Landscape of Urological Cancers
Fengye Liu1, Longfei He1, Muying Yu2
1Department of Pathophysiology, School of Basic Medical Sciences, Southwest Medical University, 646000 Luzhou, Sichuan, China.
Abstract:
Histone post-translational modifications (HPTMs) have emerged as crucial epigenetic regulators in urological malignancies, including prostate, bladder, and renal cell carcinomas. This review systematically examines four key modifications-lactylation, acetylation, methylation, and phosphorylation-and their roles in carcinogenesis. These dynamic modifications, mediated by "writers", "erasers", and "readers", influence chromatin structure and gene expression, thereby driving oncogenic processes such as metabolic reprogramming, immune evasion, and treatment resistance. The newly discovered lactylation modification links cellular metabolism to epigenetic regulation through lactate-derived histone marks, particularly in clear cell renal cell carcinoma, where it activates oncogenic pathways. Acetylation modifications, regulated by histone acetyltransferases (HATs) and histone deacetylases (HDACs), modulate chromatin accessibility and are implicated in silencing cancer suppressors. Methylation patterns, controlled by histone lysine methyltransferases (KMTs) and histone lysine demethylases (KDMs), demonstrate dual roles in gene regulation, with specific marks either promoting or suppressing carcinogenesis. Finally, phosphorylation dynamics affect critical cellular processes such as cell cycle progression and DNA repair. This review underscores the therapeutic potential of targeting these modifications, as evidenced by promising results with HDAC and Enhancer of zeste homolog 2 (EZH2) inhibitors. However, challenges persist in clinical translation, including off-target effects and the complexity of the cancer microenvironment. Future research should utilize multi-omics approaches to elucidate modification crosstalk and develop precision therapies. Overall, this comprehensive analysis provides valuable insights into the epigenetic mechanisms underlying urological cancers and highlights remaining knowledge gaps and therapeutic opportunities in this rapidly evolving field.
Insights
Histone post-translational modifications (HPTMs) regulate urological cancers by altering gene expression. Targeting these epigenetic marks, like lactylation, offers therapeutic potential but requires further research for precision treatments.
Area of Science:
- Epigenetics and Cancer Biology
- Uro-oncology
- Molecular Mechanisms of Carcinogenesis
Background:
- Histone post-translational modifications (HPTMs) are critical epigenetic regulators in urological malignancies.
- These modifications influence chromatin structure and gene expression, driving oncogenesis.
Purpose of the Study:
- To systematically review four key HPTMs: lactylation, acetylation, methylation, and phosphorylation.
- To explore their roles in the carcinogenesis of prostate, bladder, and renal cell carcinomas.
- To highlight therapeutic potential and challenges in targeting HPTMs.
Main Methods:
- Systematic review of literature on HPTMs in urological cancers.
- Analysis of the roles of "writers", "erasers", and "readers" in epigenetic regulation.
- Examination of specific modifications like lactylation, acetylation, methylation, and phosphorylation.
Main Results:
- Lactylation links metabolism to epigenetics, activating oncogenic pathways, especially in clear cell renal cell carcinoma.
- Acetylation and methylation show dual roles in gene regulation and cancer suppression.
- Phosphorylation affects cell cycle and DNA repair, while HPTMs drive metabolic reprogramming, immune evasion, and treatment resistance.
Conclusions:
- Targeting HPTMs, such as with HDAC and EZH2 inhibitors, shows therapeutic promise for urological cancers.
- Clinical translation faces challenges including off-target effects and tumor microenvironment complexity.
- Future research should employ multi-omics to understand HPTM crosstalk and develop precision therapies.
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