Glycolysis-mediated H3K18la modifications drive aggressive bladder cancer through metabolic and epigenetic reprogramming
-
By
-
Zhan Wang
-
Zhaokai Zhou
-
Shuai Yang
-
Zihao Zhao
-
Xiaozu Li
-
Xingchen Liu
-
Guangyang Cheng
-
Ran Xu
-
Qi Li
-
Dong Xing
-
June 30, 2026
-
Clinical Scorecard: Metabolic and Epigenetic Reprogramming Driven by H3K18la Modifications in Aggressive Bladder Cancer Linked to Glycolysis
At a Glance
| Category | Detail |
|---|
| Condition | Bladder Cancer |
| Key Mechanisms | Glycolysis and histone lactylation (H3K18la) linked to tumor progression. |
| Target Population | Patients with aggressive bladder cancer. |
| Care Setting | Oncology and cancer research. |
Key Highlights
- Elevated histone lactylation (H3K18la) linked to glycolysis is associated with poor prognosis in bladder cancer (BC).
- Inhibition of glycolysis or LDHA knockdown suppresses BC growth.
- H3K18la is positively correlated with the expression of key oncogenic genes (AHNAK2, PVR, SLC7A11, SREBF1).
Guideline-Based Recommendations
Diagnosis
- Assess glycolytic activity and histone lactylation levels in bladder cancer samples.
Management
- Consider targeting glycolysis and histone lactylation in therapeutic strategies for bladder cancer.
Monitoring & Follow-up
- Monitor levels of H3K18la and glycolytic activity as potential prognostic markers.
Risks
- Increased glycolytic activity and histone lactylation are associated with poor prognosis.
Patient & Prescribing Data
Patients diagnosed with aggressive bladder cancer.
Inhibition of glycolysis or LDHA may provide anti-tumor effects.
Clinical Best Practices
- Utilize single-cell RNA sequencing to identify metabolic changes in bladder cancer.
- Explore the role of lactate metabolism in the tumor microenvironment.
Related Resources & Content
