Interrupting the FGF19-FGFR4 Axis to Therapeutically Disrupt Cancer Progression

Liwei Lang, Austin Y. Shull, Yong Teng

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

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
Volume19
Issue number1
DOIs
StatePublished - Jan 1 2019

Fingerprint

Neoplasms
Fibroblast Growth Factors
Cell Proliferation
Apoptosis
Neoplasm Metastasis
Enzymes
Therapeutics

Keywords

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

ASJC Scopus subject areas

  • Oncology
  • Pharmacology
  • Drug Discovery
  • Cancer Research

Cite this

Interrupting the FGF19-FGFR4 Axis to Therapeutically Disrupt Cancer Progression. / Lang, Liwei; Shull, Austin Y.; Teng, Yong.

In: Current cancer drug targets, Vol. 19, No. 1, 01.01.2019, p. 17-25.

Research output: Contribution to journalArticle

@article{e9b52e62b1d642cebd692f6a6b59e1a6,
title = "Interrupting the FGF19-FGFR4 Axis to Therapeutically Disrupt Cancer Progression",
abstract = "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, cancer, drug development, target, β-klotho.",
author = "Liwei Lang and Shull, {Austin Y.} and Yong Teng",
year = "2019",
month = "1",
day = "1",
doi = "10.2174/1568009618666180319091731",
language = "English (US)",
volume = "19",
pages = "17--25",
journal = "Current Cancer Drug Targets",
issn = "1568-0096",
publisher = "Bentham Science Publishers B.V.",
number = "1",

}

TY - JOUR

T1 - Interrupting the FGF19-FGFR4 Axis to Therapeutically Disrupt Cancer Progression

AU - Lang, Liwei

AU - Shull, Austin Y.

AU - Teng, Yong

PY - 2019/1/1

Y1 - 2019/1/1

N2 - 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.

AB - 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.

KW - FGF19

KW - FGFR4

KW - cancer

KW - drug development

KW - target

KW - β-klotho.

UR - http://www.scopus.com/inward/record.url?scp=85057650280&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85057650280&partnerID=8YFLogxK

U2 - 10.2174/1568009618666180319091731

DO - 10.2174/1568009618666180319091731

M3 - Article

VL - 19

SP - 17

EP - 25

JO - Current Cancer Drug Targets

JF - Current Cancer Drug Targets

SN - 1568-0096

IS - 1

ER -