ReviewInternational journal of biological sciences2025
Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.
Review in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Bioactive Natural Compounds in Triple-Negative Breast Cancer: Molecular Targets and Therapeutic Perspectives.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Mitophagy and Ubiquitination Coordinate Context-Specific Mitochondrial Quality Control and EMT/MET Plasticity to Drive Cancer Cell Invasion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Dynamin 1 promotes colorectal cancer progression by activating the PI3K/Akt signaling pathway.Journal of translational medicine · 2025Article
- LAMC2 promotes gallbladder carcinoma metastasis through the TGF-β pathway.Cancer cell international · 2025Article
- SERPINE1 maintained expression by NR4A1 promotes invasion and migration of glioblastoma in hypoxic microenvironment.Frontiers in oncology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) is a fundamental biological process that promotes cancer metastasis and chemoresistance. However, the therapeutic efficacy of EMT inhibitors remains limited. Ubiquitination, a critical post-translational modification, involves attaching ubiquitin molecules to proteins to regulate their function and stability. It modulates EMT by controlling key EMT transcription factors (EMT-TFs) and associated signaling pathways. Evidence indicates that ubiquitination-dependent regulation of EMT serves as a central mechanism underlying tumor metastasis and chemoresistance. Targeting specific deubiquitinases (DUBs) or E3 ligases can effectively reverse EMT-induced cancer progression and treatment resistance. These findings highlight the therapeutic potential of E3 ligase and DUB inhibitors in oncology. Collectively, ubiquitination-regulated EMT is pivotal in mediating metastasis and chemoresistance in malignant tumors. This review summarizes the molecular mechanisms of EMT and emphasizes ubiquitination's essential role in regulating EMT to promote tumor metastasis and chemoresistance. Consequently, developing inhibitors against specific E3 ligases and DUBs offers a promising strategy to improve cancer treatment outcomes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.