Cocaine- and amphetamine- regulated transcript (CART) as a novel potential promitotic factor in prostate cancer.

Prostate cancer (PC) is a common and deadly neoplasm worldwide. Despite intensive researchs, its exact cause remains unclear. Cocaine- and amphetamine- regulated transcript (CART) is pleiotropic in function peptide, mostly found in central neurvous system and diffuse neuroendocrine system cells. It may play a role in cell division and survival via GPR160 receptor. Some studies suggest role of CART in development of various cancers, including prostate cancer. Preliminary findings suggest CART's presence in benign prostatic hyperplasia. It raises the possibility of CART involvment in prostate cancer. The main goals of our research are to determine whether CART plays role a role in pathogenesis of prostate cancer and whether CART expression varies depending on the malignancy level of the tumor. Additionally, potential associations between CART expresion levels and selected histopathological and clinical data will be estabilished

The Role of Cocaine- and Amphetamine-Regulated Transcript (CART) in Cancer: A Systematic Review

The functions of cocaine- and amphetamine-regulated transcript (CART) neuropeptide encoded by the CARTPT gene vary from modifying behavior and pain sensitivity to being an antioxidant. Putative CART peptide receptor GPR160 was implicated recently in the pathogenesis of cancer. However, the exact role of CART protein in the development of neoplasms remains unclear. This systematic review includes articles retrieved from the Scopus, PubMed, Web of Science and Medline Complete databases. Nineteen publications that met the inclusion criteria and describe the association of CART and cancer were analyzed. CART is expressed in various types of cancer, e.g., in breast cancer and neuroendocrine tumors (NETs). The role of CART as a potential biomarker in breast cancer, stomach adenocarcinoma, glioma and some types of NETs was suggested. In various cancer cell lines, CARTPT acts an oncogene, enhancing cellular survival by the activation of the ERK pathway, the stimulation of other pro-survival molecules, the inhibition of apoptosis or the increase in cyclin D1 levels. In breast cancer, CART was reported to protect tumor cells from tamoxifen-mediated death. Taken together, these data support the role of CART activity in the pathogenesis of cancer, thus opening new diagnostic and therapeutic approaches in neoplastic disorders