Published online Feb 28, 2016. doi: 10.3748/wjg.v22.i8.2415
Peer-review started: May 1, 2015
First decision: May 18, 2015
Revised: May 25, 2015
Accepted: December 8, 2015
Article in press: December 8, 2015
Published online: February 28, 2016
Processing time: 304 Days and 0.5 Hours
Fibroblast growth factor receptors (FGFRs) regulate a variety of cellular functions, from embryogenesis to adult tissue homeostasis. FGFR signaling also plays significant roles in the proliferation, invasion, and survival of several types of tumor cells. FGFR-induced alterations, including gene amplification, chromosomal translocation, and mutations, have been shown to be associated with the tumor initiation and progression of gastric cancer, especially in diffuse-type cancers. Therefore, the FGFR signaling pathway might be one of the therapeutic targets in gastric cancer. This review aims to provide an overview of the role of FGFR signaling in tumorigenesis, tumor progression, proliferation, and chemoresistance. We also discuss the accumulating evidence that demonstrates the effectiveness of using clinical therapeutic agents to inhibit FGFR signaling for the treatment of gastric cancer.
Core tip: Fibroblast growth factor receptor (FGFR) is one of the drivers signaling in the development of gastric cancer. The use of molecular agents as targets of the FGFRs pathway has currently been approved in experimental and clinical trials as a mono-targeted approach or in combination with chemotherapeutic agents. FGFRs might be a promising therapeutic target for the treatment of gastric cancer.
