Related Experiment Video

Updated: Oct 16, 2025

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
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The FOXM1/RNF26/p57 axis regulates the cell cycle to promote the aggressiveness of bladder cancer

Lu Yi1,2,3, Haohui Wang1,2,3, Wei Li1,2,3

  • 1Department of Urology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.

Cell Death & Disease
|October 15, 2021
PubMed

Insights

Researchers identified a new molecular pathway involving FOXM1, RNF26, and p57 that drives bladder cancer progression. Targeting this FOXM1/RNF26/p57 axis may offer novel therapeutic strategies for bladder cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Bioinformatics

Background:

  • Bladder cancer remains a lethal malignancy with limited improvements in survival rates.
  • Novel therapeutic targets are crucial for effective bladder cancer treatment.
  • Understanding molecular mechanisms driving bladder cancer is essential.

Purpose of the Study:

  • To investigate the role of RNF26 in bladder cancer.
  • To identify molecular pathways regulating bladder cancer progression.
  • To explore potential therapeutic targets for bladder cancer.

Main Methods:

  • Bioinformatics analysis to identify risk factors.
  • Expression analysis in bladder cancer tissues and cells.
  • Investigation of regulatory mechanisms and downstream effects.

Main Results:

  • RNF26 is identified as a risk factor and is upregulated in bladder cancer.
  • Higher RNF26 expression correlates with poor prognosis and promotes tumor progression.
  • FOXM1 upregulates RNF26 transcriptionally, which then degrades p57, promoting cell cycle progression.

Conclusions:

  • A novel FOXM1/RNF26/p57 signaling axis regulates the cell cycle in bladder cancer.
  • This axis enhances bladder cancer progression.
  • The FOXM1/RNF26/p57 pathway represents a potential therapeutic target for bladder cancer treatment.

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