Abstract
Fibroblast growth factors (FGFs) and FGF receptors (FGFRs) play an important role in the maintenance of tissue homeostasis and the development and differentiation of prostate tissue through epithelial-stromal interactions. Aberrations of this signaling are linked to the development and progression of prostate cancer (PCa). The FGF family includes two subfamilies, paracrine FGFs and endocrine FGFs. Paracrine FGFs directly bind the extracellular domain of FGFRs and act as a growth factor through the activation of tyrosine kinase signaling. Endocrine FGFs have a low affinity of heparin/heparan sulfate and are easy to circulate in serum. Their biological function is exerted as both a growth factor binding FGFRs with co-receptors and as an endocrine molecule. Many studies have demonstrated the significance of these FGFs and FGFRs in the development and progression of PCa. Herein, we discuss the current knowledge regarding the role of FGFs and FGFRs—including paracrine FGFs, endocrine FGFs, and FGFRs—in the development and progression of PCa, focusing on the representative molecules in each subfamily.
Highlights
Prostate cancer (PCa) is one of the most common hormone-dependent cancers
The Ig-like domain is crucial for determining ligand-binding specificity, and as a result, seven fibroblast growth factor (FGF) receptors (FGFRs) with different ligand-binding specificities are derived from four Fgfr genes [12]
The loss of FGFR2 isoforms is shown in human PCa tissues, and the loss of FGFR2IIIb is associated with the characteristics of castration-resistant prostate cancer (CRPC) in particular [17]
Summary
Prostate cancer (PCa) is one of the most common hormone-dependent cancers. Androgen-deprived therapy (ADT) has been the standard option for PCa. Androgen-deprived therapy (ADT) has been the standard option for PCa It is initially effective in most PCa cases; PCa becomes refractory for ADT in spite of the castration level of serum testosterone, which is called “castration-resistant prostate cancer” (CRPC). There have been multiple studies on the efficacy of various agents that include androgen-receptor (AR) targeted agents and anticancer drugs. Many studies have demonstrated the aberrant activation of fibroblast growth factor (FGF)/FGF receptor (FGFR) signaling in several cancers, including head and neck, lung, breast, endometrial, bladder, and prostate cancer [1,2]. We review the FGF family’s involvement in the development and progression of prostate cancer. We mainly discuss the representative molecules in each subfamily: FGF9 as classic FGFs, FGF19 as endocrine FGFs, and FGFR2IIIb
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