Cancer Protein Description
This report provides a detailed description of a selected cancer protein with information collected from various sources, including UniProt, the Wellcome Trust Sanger Institute’s Catalogue of Somatic Mutations in Cancer (COSMIC), and the Atlas of Genetics and Cytogenetics in Oncology and Haematology.
| Protein Name: | Cdc42 |
| Gene Name: | CDC42 |
| Protein Full Name: | Cell division control protein 42 homolog |
| Alias: | CDC42Hs; cell division cycle 42 (GTP binding protein); G25K; G25K GTP-binding protein, brain isoform; GP |
| Mass (Da): | 21311 |
| Number AA: | 191 |
| UniProt ID: | P60953 |
| Locus ID: | 998 |
| COSMIC ID: | CDC42 |
| Gene location on chromosome: | 1p36.12 |
| Cancer protein type: | OP |
| Effect of cancer mutation on protein: | UNCLEAR |
| Effect of active protein on cancer: | PROMOTES |
| Number of cancer specimens: | 20209 |
| Percent of cancer specimens with mutations: | 0.17 |
| Normal role description: | CDC42 is a monomeric G-protein of the Rho family of GTPases. CDC42 has been characterized primarily in regulating actin cytoskeletal organization and cell polarity but also has diverse roles in cell migration, chemotaxis, intracellular trafficking, endocytosis, and cell cycle progression all of which requires reorganization of actin cytoskeleton. The diverse roles of CDC42 appears to be cell type specific. During cell motility, CDC42 functions through activation of the ARP2/3 complex leading to actin polymerization and cell movement through formation of filopodia. CDC42 dependent cancer development has been suggested to be tissue specific and its suggested role in cancer progression varies greatly. Some suggested roles of CDC42 has been in promoting cell growth by preventing EGF receptor degradation, promotion of chromosome misalignment during cell division, promotion of invasion and metastasis by loss of cell polarity due to epithelial-mesenchymal transition and abberant transcriptional control caused by activation of NF-kB, STAT3 and inhibition of ID4. Overexpression of CDC42 or dysfunction of regulatory proteins appears to be the primary mechanism of CDC42 mediated cancer development. Very few mutations of CDC42 have been observed in breast and colon cancers. |
| Commentary on involvement of protein in cancer: | According to atlasofgeneticsoncology.org, CDC42 overexpression has been observed in breast cancer, testicular cancer, head and neck squamous cell carcinomas, melanomas, colorectal cancers, hepatocellular carcinomas, lung cancer, anaplastic large cell lymphoma and bladder cancer. Primarily the mechanism of development appears to be through dysfunction of regulatory proteins or overexpression of CDC42 not by mutational mechanisms. |