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The HECT family of E3 ubiquitin ligases: multiple players in cancer development Bernassola F; Karin M; Ciechanover A; Melino GCancer Cell 2008[Jul]; 14 (1): 10-21The 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.|*Signal Transduction/drug effects/genetics[MESH]|Animals[MESH]|Antineoplastic Agents/pharmacology[MESH]|Cell Transformation, Neoplastic/genetics/*metabolism[MESH]|Endosomal Sorting Complexes Required for Transport[MESH]|Enzyme Inhibitors/pharmacology[MESH]|Gene Expression Regulation, Enzymologic[MESH]|Gene Expression Regulation, Neoplastic[MESH]|Humans[MESH]|Nedd4 Ubiquitin Protein Ligases[MESH]|Neoplasms/drug therapy/*enzymology/genetics[MESH]|Repressor Proteins/metabolism[MESH]|Substrate Specificity[MESH]|Tumor Suppressor Proteins/genetics/*metabolism[MESH]|Ubiquitin-Protein Ligases/antagonists & inhibitors/genetics/*metabolism[MESH]|Ubiquitin/*metabolism[MESH] |
