Literature summary for 2.7.10.1 extracted from

Bai, L.; Yang, J.; Ok, J.; MacK, P.; Kung, H.; Evans, C.
Simultaneous targeting of Src kinase and receptor tyrosine kinase results in synergistic inhibition of renal cell carcinoma proliferation and migration (2012), Int. J. Cancer, 130, 2693-2702.

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Application

Application	Comment	Organism
medicine	effects of Src kinase inhibitor saracatinib and multiple receptor tyrosine kinase inhibitor sunitinib on renal cell carcinoma cell line ACHN and Caki-1. Saracatinib alone or in combination with sunitinib inhibits the migration of ACHN and Caki-1 cells in vitro. Combined treatment results in improved growth inhibition, greater loss of the S phase cell population and decreased clonogenic colony formation compared to sunitinib alone in the metastatic Caki-1 line. Saracatinib alone and in combination with sunitinib inhibits phosphorylation of the cell progression regulator c-Myc in a dose-dependent manner. Sunitinib alone or in combination suppresses cyclin-D1 expression with the combination showing greater dose-dependent effect. Sunitinib inhibits vascular endothelial growth factor secretion through the inhibition of STAT3 signaling and VEGF biosynthesis. HIF1-alpha expression in normoxic and hypoxic conditions in Caki-1 cells is inhibited by either saracatinib or sunitinib when administered alone, however, a greater reduction occurrs when these compounds are given in combination. Targeting Src kinase and RTK simultaneously with saracatinib and sunitinib results in 70-80% blockade of renal cell carcinoma cell migration, synergistic inhibition of cell growth and reduction of acquired drug resistance in Caki-1 cells	Homo sapiens

Inhibitors

Inhibitors	Comment	Organism	Structure
sunitinib	effects of Src kinase inhibitor saracatinib and multiple receptor tyrosine kinase inhibitor sunitinib on renal cell carcinoma cell line ACHN and Caki-1. Saracatinib alone or in combination with sunitinib inhibits the migration of ACHN and Caki-1 cells in vitro. Combined treatment results in improved growth inhibition, greater loss of the S phase cell population and decreased clonogenic colony formation compared to sunitinib alone in the metastatic Caki-1 line. Saracatinib alone and in combination with sunitinib inhibits phosphorylation of the cell progression regulator c-Myc in a dose-dependent manner. Sunitinib alone or in combination suppresses cyclin-D1 expression with the combination showing greater dose-dependent effect. Sunitinib inhibits vascular endothelial growth factor secretion through the inhibition of STAT3 signaling and VEGF biosynthesis. HIF1-alpha expression in normoxic and hypoxic conditions in Caki-1 cells is inhibited by either saracatinib or sunitinib when administered alone, however, a greater reduction occurrs when these compounds are given in combination. Targeting Src kinase and RTK simultaneously with saracatinib and sunitinib results in 70-80% blockade of renal cell carcinoma cell migration, synergistic inhibition of cell growth and reduction of acquired drug resistance in Caki-1 cells	Homo sapiens

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	-	-	-

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Release 2023.1 (January 2023)