Abstract
Cancer disease is the second leading cause of death in the world and one of the main fields of medical research. Although there is now a greater understanding of biological mechanisms of uncontrolled cell growth, invasiveness and metastasization, the multi-step process of cancer development and evolution is still incompletely understood. The inhibition of molecules activated in cancer metastasization is an hot topic in cancer research. Among the known antimetastatic genes, KiSS-1 is involved in the metastatic cascade by preventing growth of metastasis. Moreover, loss of KiSS-1 protein expression by tumor cells has been associated with a more aggressive phenotype. KiSS-1 gene encodes a 145-amino acid protein, which following proteolytic cleavage, generates a family of kisspeptins (Kp-10, -13, and -14), that are endogenous agonists for the G-protein-coupled receptor (GPR54). The antitumor effect of KiSS-1 was primarily associated with the inhibition of proliferation, migration and cell invasion and, consequently, the reduced formation of metastasis and intratumoral microvessels. In this review, we highlight the latest data on the role of kisspeptin signaling in the suppression of metastasis in various cancer types and the use modulators of KiSS/GPR54 signaling as potential novel therapeutic agents for the treatment of cancer.
Highlights
Cancer is defined as a heterogeneous group of diseases, characterized by uncontrolled cell growth
Metastasization is the process through which primary tumor cells colonize distant second sites: a tumor cell that grows in a microenvironment, in order to become able to move and proliferate in another location, begins a chain of events defined as a “metastatic waterfall.”
Tumor cells are characterized by epithelial to mesenchymal transition (EMT), a complex biological and morphological change that reduce their dependency from intracellular connection
Summary
Cancer is defined as a heterogeneous group of diseases, characterized by uncontrolled cell growth. Metastasization is the process through which primary tumor cells colonize distant second sites: a tumor cell that grows in a microenvironment, in order to become able to move and proliferate in another location, begins a chain of events defined as a “metastatic waterfall.”. Uncontrolled cell growth and tumor progression are the result of a multi-step complex process including inactivation of tumor suppressor genes. Tumor cells are characterized by epithelial to mesenchymal transition (EMT), a complex biological and morphological change that reduce their dependency from intracellular connection. Mesenchymal tumor cells are able to infiltrate distant organs escaping the recognition from the immune system, until they create a macroscopic mass in second sites [2]
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