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Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance

Shuai Xiao1,2, Lingli Tian1,2, Xiaoli Gan3

  • 1National "111" Center for Cellular Regulation and Molecular Pharmaceutics, Hubei University of Technology, Wuhan 430068, China.

International Journal of Biological Sciences
|November 10, 2025
PubMed

Insights

Targeting ubiquitination, a key process in epithelial-mesenchymal transition (EMT), can combat cancer metastasis and chemoresistance. Inhibiting specific E3 ligases and deubiquitinases offers a promising therapeutic strategy for improving cancer treatment outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Epithelial-mesenchymal transition (EMT) drives cancer metastasis and chemoresistance.
  • Current EMT inhibitors have limited therapeutic efficacy.
  • Ubiquitination, a post-translational modification, regulates protein function and stability.

Purpose of the Study:

  • To review the molecular mechanisms of EMT.
  • To emphasize ubiquitination's role in regulating EMT.
  • To highlight therapeutic strategies targeting ubiquitination in cancer.

Main Methods:

  • Literature review of EMT and ubiquitination.
  • Analysis of ubiquitination's role in EMT-TFs and signaling pathways.
  • Examination of therapeutic potential of E3 ligase and DUB inhibitors.

Main Results:

  • Ubiquitination critically modulates EMT by controlling EMT-TFs and signaling pathways.
  • Ubiquitination-dependent EMT regulation is central to tumor metastasis and chemoresistance.
  • Targeting deubiquitinases (DUBs) or E3 ligases can reverse EMT-induced progression and resistance.

Conclusions:

  • Ubiquitination-regulated EMT is pivotal in mediating metastasis and chemoresistance.
  • Inhibitors of specific E3 ligases and DUBs show therapeutic promise in oncology.
  • Developing these inhibitors is a promising strategy to improve cancer treatment outcomes.
Keywords:
Drug resistanceEpithelial-mesenchymal transitionUbiquitinationtumor metastasis

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