Coordination between the amplification of the fibroblast growth factor FGF19, overexpression
of its corresponding receptor FGFR4, and hyperactivation of the downstream transmembrane
enzyme β-klotho has been found to play pivotal roles in mediating tumor development and
progression. Aberrant FGF19-FGFR4 signaling has been implicated in driving specific tumorigenic
events including cancer cell proliferation, apoptosis resistance, and metastasis by activating a myriad
of downstream signaling cascades. As an attractive target, several strategies implemented to disrupt
the FGF19-FGFR4 axis have been developed in recent years, and FGF19-FGFR4 binding inhibitors
are being intensely evaluated for their clinical use in treating FGF19-FGFR4 implicated cancers.
Based on the established work, this review aims to detail how the FGF19-FGFR4 signaling pathway
plays a vital role in cancer progression and why disrupting communication between FGF19 and
FGFR4 serves as a promising therapeutic strategy for disrupting cancer progression.
Keywords: FGF19, FGFR4, β-klotho, cancer, target, drug development.
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