Mini Review ARTICLE
Controversial role of Kisspeptins/KiSS-1R signaling system in tumor development
- 1Istituto Nazionale Tumori Fondazione G. Pascale (IRCCS), Italy
- 2DISIST, Università degli Studi di Napoli Parthenope, Italy
KiSS-1 was first described as a metastasis suppressor gene in malignant melanoma. KiSS-1 encodes a 145 amino-acid residue peptide that is further processed, producing the 54 amino acid metastin and shorter peptides collectively named kisspeptins, (KPs). KPs bind and activate KiSS-1R (GPR54). Although the Kisspeptin system has been extensively studied for its role in endocrinology of reproductive axis in mammalian, its role in cancer is still controversial. Experimental evidences show that Kisspeptin system exerts an anti-metastatic effect by the regulation of cellular migration and invasion in several cancer types. However, the role of KPs/KiSS-1R is very complex. Genomic studies suggest that KiSS-1/KiSS-1R expression might be different in the various stages of tumor development. Furthermore, overexpression of KiSS-1R has been reported to elicit drug resistance in triple negative breast cancer (TNBC). In this review we focused on multiple functions exerted by the Kisspeptins/KiSS-1R system in regulating tumor progression.
Keywords: Kisspeptin, Kiss1-R, tumor development, tumor invasion, metastasis
Received: 15 Jan 2018;
Accepted: 09 Apr 2018.
Edited by:SILVIA FASANO, Università degli Studi della Campania "Luigi Vanvitelli" Caserta, Italy
Reviewed by:Satoshi Ogawa, Monash University Malaysia, Malaysia
Antimo Migliaccio, Università degli Studi della Campania "Luigi Vanvitelli" Naples, Italy
Floriana Morgillo, Università degli Studi della Campania "Luigi Vanvitelli" Naples, Italy
Copyright: © 2018 Fratangelo, Carriero and Motti. 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 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. Maria Letizia Motti, Università degli Studi di Napoli Parthenope, DISIST, Via Acton, 38, Naples, 80122, Italy, firstname.lastname@example.org