Glycolysis-mediated H3K18la modifications drive aggressive bladder cancer through metabolic and epigenetic reprogramming - Takeaways - MDSpire

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

  • 0 min

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  • 1

    Histone lactylation (H3K18la) and glycolytic activity are significantly elevated in aggressive bladder cancer, correlating with poor patient prognosis.

  • 2

    Inhibition of glycolysis or knockdown of lactate dehydrogenase A (LDHA) suppresses bladder cancer growth in both in vitro and in vivo models.

  • 3

    Four oncogenic target genes (AHNAK2, PVR, SLC7A11, SREBF1) were identified as being associated with H3K18la and linked to bladder cancer progression.

  • 4

    The study highlights the connection between lactate metabolism and epigenetic regulation in bladder cancer, suggesting potential therapeutic targets.

  • 5

    Single-cell RNA sequencing analysis revealed significant metabolic reprogramming in bladder cancer, emphasizing the role of histone lactylation.

Original Source(s)

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

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