Checks and balances: interplay of RTKs and PTPs in cancer progression |
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| Authors: | Sastry Sarita K Elferink Lisa A |
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| Affiliation: | aDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555, United States;bDepartment of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, TX 77555, United States;cUTMB Comprehensive Cancer Center, University of Texas Medical Branch, Galveston, TX 77555, United States |
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| Abstract: | In recent years, targeted therapies for receptor tyrosine kinases (RTKs) have shown initial promise in the clinical setting for the treatment of several tumors driven by these oncogenic signaling pathways. Unfortunately, clinical relapse due to acquired resistance to these molecular therapeutics is common. An improved understanding of how tumors bypass the inhibitory effects of RTK-targeted therapies has revealed a rich myriad of possible mechanisms for acquired resistance. Protein tyrosine phosphatases (PTPs) can function as oncogenes or tumor suppressors to either enhance or suppress RTK signaling. Recent studies suggest that the loss or gain of function of PTP's can significantly impinge on RTK signaling during tumor progression. Here we review the interplay between RTKs and PTPs as an emerging mechanism for acquired resistance to RTK-targeted therapies, that may aid in the design of improved therapies to prevent and overcome resistance in treatments for cancer patients. |
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| Keywords: | Abbreviations: Cag A, cytotoxin associated antigen A DUSP, dual specificity phosphatase EGF, epidermal growth factor EGFR, EGF receptor ErbBs, epidermal growth factor receptor family of receptor tyrosine kinases FAK, focal adhesion kinase FGFR, fibroblast growth factor receptor HGF, hepatocyte growth factor IGF-1R, type 1 insulin-like growth factor receptor MEF, mouse embryonic fibroblast Met, HGF receptor PI3K, phosphatidylinositol 3-kinase PIP2, phosphatidylinositol 4,5,-bisphosphate PIP3, 3,4,5,-triphosphate PTEN, phosphatase and tensin homolog deleted on chromosome 10 PTP, protein tyrosine phosphatases NSCLC, non-small cell lung carcinoma PDGF, platelet derived growth factor PDGFR, PDGF receptor RTK, receptor tyrosine kinase SH2, src homology 2 shRNA, small hairpin RNA SNP, single nucleotide polymorphisms STAM2, signal transducing adaptor molecule 2 TKI, tyrosine kinase inhibitor VEGF, vascular endothelial growth factor VEGFR, VEGF receptor |
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