Proof-of-concept study investigating the role of S100P-RAGE in nasopharyngeal carcinoma

xlomafota13 shared this article with you from Inoreader Proof-of-concept study investigating the role of S100P-RAGE in nasopharyngeal carcinoma Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):470. doi: 10.3892/etm.2021.9901. Epub 2021 Mar 8. ABSTRACT Nasopharyngeal carcinoma (NPC) is an epithelial carcinoma that arises from the lining of the nasopharyngeal mucosa. The efficacy of radiation therapy is limited due to radiation resistance, particularly in the advanced stages of NPC. The S100P protein is a small isoform of the S100 protein family, which is involved in the regulation of various intracellular and extracellular processes, including proliferation, differentiation and intracellular signaling. The aim of the current study was to investigate the significance of the S100P-RAGE axis in NPC progression. The expression levels of S100P and receptor for activated glycation end-products (RAGE) in NPC specimens were determined by western blotting. In addition, the effect of the S100P-RAGE axis on NPC was evaluated in vitro by proliferation and migration assays using C666-1 cells treated wit h S100P or the RAGE inhibitor FPS-ZM1. The underlying mechanism was also investigated by western blotting. The expression of S100P and RAGE was detected in clinical specimens from 15 patients with NPC and 15 patients with benign nasopharyngeal inflammation, and was observed to be higher in NPC tissues compared with inflamed tissues. Furthermore, the interaction of S100P with RAGE increased the proliferation and migration potential of C666-1 cells, and activated mitogen-activated protein kinase and NF-κB signaling. These results indicate that the S100P-RAGE axis exerts a promoting effect on the progression of NPC. Therefore therapeutic strategies targeting S100P-RAGE merit further exploration for the treatment of NPC. PMID:33767765 | PMC:PMC7976439 | DOI:10.3892/etm.2021.9901 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.