The HECT Family of E3 Ubiquitin Ligases: Multiple Players in Cancer Development

The involvement of the homologous to E6-AP carboxyl terminus (HECT)-type E3s in crucial signaling pathways implicated in tumorigenesis is presently an area of intense research and extensive scientific interest. This review highlights recent discoveries on the ubiquitin-mediated degradation of crucia...

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Veröffentlicht in:	Cancer cell 2008-07, Vol.14 (1), p.10-21
Hauptverfasser:	Bernassola, Francesca, Karin, Michael, Ciechanover, Aaron, Melino, Gerry
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antineoplastic Agents - pharmacology Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Endosomal Sorting Complexes Required for Transport Enzyme Inhibitors - pharmacology Gene Expression Regulation, Enzymologic Gene Expression Regulation, Neoplastic Humans Nedd4 Ubiquitin Protein Ligases Neoplasms - drug therapy Neoplasms - enzymology Neoplasms - genetics Repressor Proteins - metabolism Signal Transduction - drug effects Signal Transduction - genetics Substrate Specificity Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism Ubiquitin - metabolism Ubiquitin-Protein Ligases - antagonists & inhibitors Ubiquitin-Protein Ligases - genetics Ubiquitin-Protein Ligases - metabolism
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Zusammenfassung:	The involvement of the homologous to E6-AP carboxyl terminus (HECT)-type E3s in crucial signaling pathways implicated in tumorigenesis is presently an area of intense research and extensive scientific interest. This review highlights recent discoveries on the ubiquitin-mediated degradation of crucial tumor suppressor molecules catalyzed by the HECT-type E3s. By providing a portrait of their protein targets, we intend to link the substrate specificity of HECT-type E3s with their contribution to tumorigenesis. Moreover, we discuss the relevance of targeting the HECT E3s, through the development of small-molecule inhibitors, as an anticancer therapeutic strategy.
ISSN:	1535-6108 1878-3686
DOI:	10.1016/j.ccr.2008.06.001