Targeting Drugs Against Fibroblast Growth Factor(s)-Induced Cell Signaling

Agrawal, Shilpi; Maity, Sanhita; AlRaawi, Zeina; Al-Ameer, Musaab; Kumar, Thallapuranam Krishnaswamy Suresh

doi:10.2174/1389450121999201012201926

Targeting Drugs Against Fibroblast Growth Factor(s)-Induced Cell Signaling

Journal Article · Wed Feb 17 04:00:00 EST 2021 · Current Drug Targets (Print)

DOI:https://doi.org/10.2174/1389450121999201012201926· OSTI ID:1849367

Agrawal, Shilpi ^[1]; Maity, Sanhita ^[2]; AlRaawi, Zeina ^[2]; Al-Ameer, Musaab ^[2]; ^[2]

Department of Chemistry and Biochemistry, University of Arkansas, Fayetteville, Arkansas, United States; OSTI
Department of Chemistry and Biochemistry, University of Arkansas, Fayetteville, Arkansas, United States

Background::

The fibroblast growth factor (FGF) family is comprised of 23 highly regulatedmonomeric proteins that regulate a plethora of developmental and pathophysiological processes,including tissue repair, wound healing, angiogenesis, and embryonic development. Binding ofFGF to fibroblast growth factor receptor (FGFR), a tyrosine kinase receptor, is facilitated by a glycosaminoglycan,heparin. Activated FGFRs phosphorylate the tyrosine kinase residues that mediateinduction of downstream signaling pathways, such as RAS-MAPK, PI3K-AKT, PLCγ, andSTAT. Dysregulation of the FGF/FGFR signaling occurs frequently in cancer due to gene amplification,FGF activating mutations, chromosomal rearrangements, integration, and oncogenic fusions.Aberrant FGFR signaling also affects organogenesis, embryonic development, tissue homeostasis,and has been associated with cell proliferation, angiogenesis, cancer, and other pathophysiologicalchanges.

Objective::

This comprehensive review will discuss the biology, chemistry, and functions of FGFs,and its current applications toward wound healing, diabetes, repair and regeneration of tissues, andfatty liver diseases. In addition, specific aberrations in FGFR signaling and drugs that target FGFRand aid in mitigating various disorders, such as cancer, are also discussed in detail.

Conclusion::

Inhibitors of FGFR signaling are promising drugs in the treatment of several types ofcancers. The clinical benefits of FGF/FGFR targeting therapies are impeded due to the activationof other RTK signaling mechanisms or due to the mutations that abolish the drug inhibitory activityon FGFR. Thus, the development of drugs with a different mechanism of action for FGF/FGFRtargeting therapies is the recent focus of several preclinical and clinical studies.

Research Organization:: Univ. of Arkansas, Fayetteville, AR (United States)

Sponsoring Organization:: USDOE Office of Science (SC)

DOE Contract Number:: FG02-01ER15161

OSTI ID:: 1849367

Journal Information:: Current Drug Targets (Print), Journal Name: Current Drug Targets (Print) Journal Issue: 2 Vol. 22; ISSN 1389-4501

Country of Publication:: United States

Language:: English

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