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| Substrate | Role in cancer |
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| Jagged 1 (JAG1) [72, 73] | JAG1 is a ligand for Notch receptors and is a target for colon, breast, cervical, ovarian, and hematological cancers [167]. |
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| Glypican-1 (GLP1) [76] | Downregulation of GPC1 in pancreatic cancer cells resulted in attenuated tumor growth, angiogenesis, and metastasis in vivo. Angiogenesis and metastasis were decreased in GPC1 knockout mice following intrapancreatic implantation with human pancreatic cancer cells [74]. |
|
| Vasorin [77] | Vasorin directly binds to transforming growth factor (TGF) β and attenuates TGFβ signaling in vitro. Overexpression of vasorin leads to the attenuation of TGFβ signaling through the generation of the soluble form. |
|
| Neuregulin 1 [82] | Neuregulins are expressed in a significant subset of patients with breast cancer and their presence correlates with clinical response to certain antitumoral treatments such as trastuzumab [83]. |
| Overexpression of neuregulins in the mammary tissue results in the generation of adenocarcinomas in MCF7 breast cancer cells. In addition, reduction of neuregulin by the use of antisense oligonucleotides reduces tumorigenesis and metastasis [80]. |
|
| Trop2 [87, 168] | Trop2 is upregulated in tumors and correlates with increased aggressiveness and metastasis [84, 85]. |
| Trop2 Fab inhibits the growth of breast cancer xenografts [86]. |
|
| Carbonic anhydrase IX(CA IX) [89, 90] | CA IX is the most widely expressed gene in response to hypoxia and is connected with the increase of the aggressive/invasive phenotype of tumors [88]. |
| Its expression is closely related to prognosis of the clinical outcome in several tumor types [88]. |
|
| FLT-1 [93] vascular endothelial growth factor receptor 1 (VEGFR1) | FLT1 inhibition reduces tumor metastasis, suggesting that it represents a therapeutic target in metastatic disease [91]. |
| Inhibition of tumor angiogenesis, arthritis, and atherosclerosis by anti-Flt1 [92]. |
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| C MET receptor [95, 96] | Activating mutations were discovered in the c-MET kinase domain in both sporadic and inherited forms of cancer [97]. |
| CMET is involved in proliferation, motility, migration, and invasion [169, 170]. |
|
| Protein tyrosine phosphatase alpha (PTPα) [101] | PTPα promotes integrin-stimulated cell migration. PTPα binds to RACK1, which is a molecular scaffold protein that integrates integrin and growth factor signaling. Binding stimulates IGF-1 to phosphorylate PTPα to promote cell migration [100]. |
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