Fibroblast Growth Factor Receptors (FGFRs) and Noncanonical Partners in Cancer Signaling
Autor: | Chiara Francavilla, Harriet R. Ferguson, Michael P. Smith |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
musculoskeletal diseases animal structures Carcinogenesis QH301-705.5 extracellular matrix EGFR FGFs Review Biology Fibroblast growth factor medicine.disease_cause Receptor tyrosine kinase cell adhesion molecules 03 medical and health sciences 0302 clinical medicine Neoplasms medicine Humans cancer Receptor Fibroblast Growth Factor Type 1 Receptor Fibroblast Growth Factor Type 2 Biology (General) Fibroblast growth factor receptor 1 Cancer General Medicine medicine.disease coreceptors tumorigenesis 030104 developmental biology Fibroblast growth factor receptor FGFRs 030220 oncology & carcinogenesis Cancer cell embryonic structures receptor tyrosine kinase Cancer research biology.protein Signal transduction biological phenomena cell phenomena and immunity signaling |
Zdroj: | Cells, Vol 10, Iss 1201, p 1201 (2021) Cells |
ISSN: | 2073-4409 |
Popis: | Increasing evidence indicates that success of targeted therapies in the treatment of cancer is context-dependent and is influenced by a complex crosstalk between signaling pathways and between cell types in the tumor. The Fibroblast Growth Factor (FGF)/FGF receptor (FGFR) signaling axis highlights the importance of such context-dependent signaling in cancer. Aberrant FGFR signaling has been characterized in almost all cancer types, most commonly non-small cell lung cancer (NSCLC), breast cancer, glioblastoma, prostate cancer and gastrointestinal cancer. This occurs primarily through amplification and over-expression of FGFR1 and FGFR2 resulting in ligand-independent activation. Mutations and translocations of FGFR1-4 are also identified in cancer. Canonical FGF-FGFR signaling is tightly regulated by ligand-receptor combinations as well as direct interactions with the FGFR coreceptors heparan sulfate proteoglycans (HSPGs) and Klotho. Noncanonical FGFR signaling partners have been implicated in differential regulation of FGFR signaling. FGFR directly interacts with cell adhesion molecules (CAMs) and extracellular matrix (ECM) proteins, contributing to invasive and migratory properties of cancer cells, whereas interactions with other receptor tyrosine kinases (RTKs) regulate angiogenic, resistance to therapy, and metastatic potential of cancer cells. The diversity in FGFR signaling partners supports a role for FGFR signaling in cancer, independent of genetic aberration. |
Databáze: | OpenAIRE |
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