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Updated: Jan 13, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
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UBR5 regulates the progression of colorectal cancer cells through Snail-induced epithelial-mesenchymal transition

Xinyue Zhao1, Ruiying Liu1, Zhihui Han1

  • 1Edmond H. Fischer Signal Transduction Laboratory, School of Life Sciences, Jilin University, Changchun, Jilin 130012, China.

Genes & Diseases
|January 6, 2026
PubMed

Insights

The E3 ubiquitin ligase UBR5 degrades Snail, a key inducer of epithelial-to-mesenchymal transition (EMT). This UBR5-Snail interaction inhibits colorectal cancer progression and metastasis.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Snail is a crucial transcription factor that drives epithelial-to-mesenchymal transition (EMT), a process implicated in cancer progression and metastasis.
  • Understanding the post-translational regulation of Snail is essential for developing targeted cancer therapies.

Purpose of the Study:

  • To investigate the role of UBR5 (a ubiquitin ligase) in regulating Snail protein stability and its impact on colorectal cancer (CRC) progression.
  • To elucidate the molecular mechanism by which UBR5 controls Snail and its downstream effects on EMT and CRC metastasis.

Main Methods:

  • In vitro binding assays to assess UBR5-Snail interaction.
  • Western blotting to analyze Snail protein levels upon UBR5 modulation (depletion or overexpression).
  • Cellular assays to evaluate EMT markers, cell invasion, and tumor progression in colorectal cancer cells.
  • Analysis of UBR5 expression in human colorectal cancer tissues and correlation with patient prognosis.

Main Results:

  • UBR5 directly binds to Snail and promotes its ubiquitin-mediated degradation, a process dependent on Snail phosphorylation.
  • Depletion of UBR5 leads to Snail accumulation, enhanced EMT, and increased invasion in colorectal cancer cells.
  • Overexpression of UBR5 reduces Snail levels and cellular invasiveness, while an inactive UBR5 mutant fails to regulate Snail and EMT.
  • UBR5 is downregulated in colorectal cancer tissues, and its high expression correlates with a better prognosis.

Conclusions:

  • The UBR5-Snail axis represents a novel mechanism for post-translational regulation of EMT in colorectal cancer.
  • UBR5 acts as a tumor suppressor by degrading Snail, thereby inhibiting EMT and metastasis in colorectal cancer.
  • UBR5 levels can serve as a prognostic biomarker in colorectal cancer, with higher expression indicating a more favorable outcome.
Keywords:
Colorectal cancerEMTMetastasisSnailUBR5

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