Interrupting the FGF19-FGFR4 Axis to Therapeutically Disrupt Cancer Progression

Liwei Lang, Austin Y. Shull, Yong Teng

Research output: Contribution to journalReview articlepeer-review

9 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)17-25
Number of pages9
JournalCurrent cancer drug targets
Issue number1
StatePublished - Jan 1 2019


  • cancer
  • drug development
  • FGF19
  • FGFR4
  • target
  • β-klotho.

ASJC Scopus subject areas

  • Oncology
  • Pharmacology
  • Drug Discovery
  • Cancer Research


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