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Front. Genet. | doi: 10.3389/fgene.2019.00012

Swapping the Residential FGFR2 to Ectopic FGFR1 Signaling Axis Contributes to Prostate Cancer Progression

Cong Wang1,  Ziying Liu1, Yuepeng Ke2 and  Fen Wang2*
  • 1Wenzhou Medical University, China
  • 2Texas A&M University, United States

Advanced castrate-resistant prostate cancer (CRPC) is a poorly prognostic disease with no effective cures currently. Understanding the molecular mechanism that underlies the initiation and progression of CRPC will provide new strategies for this deadly disease. One candidate pathway is the fibroblast growth factor (FGF) signaling axis. Loss of the resident FGF7/FGF10-type 2 FGF receptor (FGFR2) pathway and gain of the ectopic type 1 FGF receptor (FGFR1) pathways are associated with the progression to malignancy in prostate cancer (PCa) and many other epithelial originated lesions. Although FGFR1 and FGFR2 share similar amino acid sequences and structure domains, the two transmembrane tyrosine kinases elicit distinctive, even sometime opposite signals in cells. Recent studies have revealed that the ectopic FGFR1 signaling pathway promotes PCa progression via multiple mechanisms, including promoting tumor angiogenesis, reprogramming cancer cell metabolism, and potentiating inflammation in the tumor microenvironment. Thus, suppression of FGFR1 signaling can be an effective novel strategy to treat CRPC.

Keywords: growth factor, receptor tyrosine kinase, Prostate, Cancer Progression, Cell signaling

Received: 21 Nov 2018; Accepted: 11 Jan 2019.

Edited by:

Saverio Bellusci, University of Giessen, Germany

Reviewed by:

Richard Grose, Queen Mary University of London, United Kingdom
David Ornitz, Washington University in St. Louis, United States  

Copyright: © 2019 Wang, Liu, Ke and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Fen Wang, Texas A&M University, College Station, United States, fwang@ibt.tamhsc.edu