Abstract
Epithelial-mesenchymal transition (EMT) plays an important role in the development of tumor metastases by facilitating cell migration and invasion. One of the hallmarks of EMT is the diminished expression of E-cadherin and gain of mesenchymal traits, which are regulated by core EMT-inducing transcriptional factors (EMT-TFs), such as Snail/Slug, ZEB1/ZEB2, and Twist1. EMT-TFs are known to be extremely labile proteins, and their protein levels are tightly controlled by the ubiquitin-proteasome system (UPS). Several E3 ubiquitin ligases have been shown to play crucial roles in the regulation of EMT, and genetic aberrations and alterations in these ligases have been detected in human cancer. In this review, we focused on EMT-TFs, describing the UPS controlling their activities and functions in cancer. A deeper understanding of the role of UPS in the regulation of EMT will provide valuable information for the development of effective anti-metastatic drugs to modulate the malignant processes mediated by EMT.
Keywords: Deubiquitinase (DUB), E3 ubiquitin ligase, epithelial-mesenchymal transition (EMT), Snail, Slug, Twist, ubiquitinproteasome system (UPS), ZEB.
Current Cancer Drug Targets
Title:Regulation of Epithelial-Mesenchymal Transition by E3 Ubiquitin Ligases and Deubiquitinase in Cancer
Volume: 16 Issue: 2
Author(s): Yasumichi Inoue, Yuka Itoh, Koichi Sato, Fumihiro Kawasaki, Chihiro Sumita, Takahito Tanaka, Daisuke Morishita and Hidetoshi Hayashi
Affiliation:
Keywords: Deubiquitinase (DUB), E3 ubiquitin ligase, epithelial-mesenchymal transition (EMT), Snail, Slug, Twist, ubiquitinproteasome system (UPS), ZEB.
Abstract: Epithelial-mesenchymal transition (EMT) plays an important role in the development of tumor metastases by facilitating cell migration and invasion. One of the hallmarks of EMT is the diminished expression of E-cadherin and gain of mesenchymal traits, which are regulated by core EMT-inducing transcriptional factors (EMT-TFs), such as Snail/Slug, ZEB1/ZEB2, and Twist1. EMT-TFs are known to be extremely labile proteins, and their protein levels are tightly controlled by the ubiquitin-proteasome system (UPS). Several E3 ubiquitin ligases have been shown to play crucial roles in the regulation of EMT, and genetic aberrations and alterations in these ligases have been detected in human cancer. In this review, we focused on EMT-TFs, describing the UPS controlling their activities and functions in cancer. A deeper understanding of the role of UPS in the regulation of EMT will provide valuable information for the development of effective anti-metastatic drugs to modulate the malignant processes mediated by EMT.
Export Options
About this article
Cite this article as:
Inoue Yasumichi, Itoh Yuka, Sato Koichi, Kawasaki Fumihiro, Sumita Chihiro, Tanaka Takahito, Morishita Daisuke and Hayashi Hidetoshi, Regulation of Epithelial-Mesenchymal Transition by E3 Ubiquitin Ligases and Deubiquitinase in Cancer, Current Cancer Drug Targets 2016; 16 (2) . https://dx.doi.org/10.2174/1568009616666151112122126
DOI https://dx.doi.org/10.2174/1568009616666151112122126 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Treatment of CNS Malignancies with a Recombinant Oncolytic Poliovirus
Drug Design Reviews - Online (Discontinued) Editorial (Thematic Issue: Chemical and Biological Technology for In Vivo and Molecular Imaging)
Current Topics in Medicinal Chemistry Targeting the L-Arginine-Nitric Oxide Pathway for Cancer Treatment
Current Pharmaceutical Design Expression of P-gp in Glioblastoma: What we can Learn from Brain Development
Current Pharmaceutical Design Matrix Metalloproteinases: New Routes to the Use of MT1-MMP As A Therapeutic Target in Angiogenesis-Related Disease
Current Pharmaceutical Design Metabolism of the Endocannabinoids Anandamide and 2-Arachidonoyl Glycerol, A Review, with Emphasis on the Pharmacology of Fatty Acid Amide Hydrolase, A Possible Target for the Treatment of Neurodegenerative Diseases and Pain
Current Medicinal Chemistry - Central Nervous System Agents Integrative Analysis of miRNA-mediated Competing Endogenous RNA Network Reveals the lncRNAs-mRNAs Interaction in Glioblastoma Stem Cell Differentiation
Current Bioinformatics Human Microdialysis
Current Pharmaceutical Biotechnology Blockade of Ser16-Hsp20 Phosphorylation Attenuates Neuroprotection Dependent Upon Bcl-2 and Bax
Current Neurovascular Research Advanced Micro-Nano-Bio Systems for Future Targeted Therapies
Current Nanoscience Aptamers: Selection, Modification and Application to Nervous System Diseases
Current Medicinal Chemistry Recent Advances in Superparamagnetic Iron Oxide Nanoparticles for Cellular Imaging and Targeted Therapy Research
Current Pharmaceutical Design Blockage of Autophagy in C6 Glioma Cells Enhanced Radiosensitivity Possibly by Attenuating DNA-PK-Dependent DSB Due to Limited Ku Nuclear Translocation and DNA Binding
Current Molecular Medicine Targeting Chemokine Receptor CXCR4 for Treatment of HIV-1 Infection, Tumor Progression, and Metastasis
Current Topics in Medicinal Chemistry Reduced Nicotinamide Adenine Dinucleotide (NADH) Fluorescence for the Detection of Cell Death
Anti-Cancer Agents in Medicinal Chemistry Nanomedicine: Magnetic Nanoparticles and their Biomedical Applications
Current Medicinal Chemistry Cancer Therapy: Targeting Cell Cycle Regulators
Anti-Cancer Agents in Medicinal Chemistry The Complex Biology of FOXO
Current Drug Targets Editorial (Thematic Issue: PET/CT in External Beam Radiation Therapy Dose Planning)
Current Radiopharmaceuticals DNMT Inhibitors in Cancer, Current Treatments and Future Promising Approach: Inhibition of Specific DNMT-Including Complexes
Epigenetic Diagnosis & Therapy (Discontinued)