Dysregulation of ubiquitin ligases in cancer

Ubiquitin ligases (UBLs) are critical components of the ubiquitin proteasome system (UPS), which governs fundamental processes regulating normal cellular homeostasis, metabolism, and cell cycle in response to external stress signals and DNA damage. Among multiple steps of the UPS system required to...

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Veröffentlicht in:Drug resistance updates Jg. 23; S. 1 - 11
Hauptverfasser: Qi, Jianfei, Ronai, Ze’ev A.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Scotland Elsevier Ltd 01.11.2015
Schlagworte:
Antineoplastic Agents - therapeutic use
Cell Cycle - genetics
Cell Transformation, Neoplastic - genetics
Cell Transformation, Neoplastic - metabolism
Cell Transformation, Neoplastic - pathology
Epigenesis, Genetic
Gene Expression Regulation, Neoplastic
Hematology, Oncology and Palliative Medicine
Humans
Infectious Disease
Neoplasms - drug therapy
Neoplasms - genetics
Neoplasms - metabolism
Neoplasms - pathology
Oncogene Proteins - genetics
Oncogene Proteins - metabolism
Proteasome Endopeptidase Complex - genetics
Proteasome Endopeptidase Complex - metabolism
Protein Processing, Post-Translational
Proteolysis
Signal Transduction
Tumor Suppressor Proteins - genetics
Tumor Suppressor Proteins - metabolism
Ubiquitin - genetics
Ubiquitin - metabolism
Ubiquitin-Protein Ligases - genetics
Ubiquitin-Protein Ligases - metabolism
Ubiquitination
ISSN:1368-7646, 1532-2084, 1532-2084
Online-Zugang:Volltext
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Zusammenfassung:Ubiquitin ligases (UBLs) are critical components of the ubiquitin proteasome system (UPS), which governs fundamental processes regulating normal cellular homeostasis, metabolism, and cell cycle in response to external stress signals and DNA damage. Among multiple steps of the UPS system required to regulate protein ubiquitination and stability, UBLs define specificity, as they recognize and interact with substrates in a temporally- and spatially-regulated manner. Such interactions are required for substrate modification by ubiquitin chains, which marks proteins for recognition and degradation by the proteasome or alters their subcellular localization or assembly into functional complexes. UBLs are often deregulated in cancer, altering substrate availability or activity in a manner that can promote cellular transformation. Such deregulation can occur at the epigenetic, genomic, or post-translational levels. Alterations in UBL can be used to predict their contributions, affecting tumor suppressors or oncogenes in select tumors. Better understanding of mechanisms underlying UBL expression and activities is expected to drive the development of next generation modulators that can serve as novel therapeutic modalities. This review summarizes our current understanding of UBL deregulation in cancer and highlights novel opportunities for therapeutic interventions.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
ISSN:1368-7646
1532-2084
1532-2084
DOI:10.1016/j.drup.2015.09.001