Non-enzymatic glycoxidation linked with nutrition enhances the tumorigenic capacity of prostate cancer epithelia through AGE mediated activation of RAGE in cancer associated fibroblasts.

Autor:	Krisanits BA; Department of Pathology & Laboratory Medicine, Medical University of South Carolina (MUSC), BEB407, Charleston, SC 29425, United States., Woods P; Department of Pathology & Laboratory Medicine, Medical University of South Carolina (MUSC), BEB407, Charleston, SC 29425, United States., Nogueira LM; Department of Pathology & Laboratory Medicine, Medical University of South Carolina (MUSC), BEB407, Charleston, SC 29425, United States., Woolfork DD; Department of Pathology & Laboratory Medicine, Medical University of South Carolina (MUSC), BEB407, Charleston, SC 29425, United States., Lloyd CE; Department of Pathology & Laboratory Medicine, Medical University of South Carolina (MUSC), BEB407, Charleston, SC 29425, United States., Baldwin A; Department of Pathology & Laboratory Medicine, Medical University of South Carolina (MUSC), BEB407, Charleston, SC 29425, United States., Frye CC; Department of Pathology & Laboratory Medicine, Medical University of South Carolina (MUSC), BEB407, Charleston, SC 29425, United States., Peterson KD; Department of Pathology & Laboratory Medicine, Medical University of South Carolina (MUSC), BEB407, Charleston, SC 29425, United States., Cosh SD; Department of Pathology & Laboratory Medicine, Medical University of South Carolina (MUSC), BEB407, Charleston, SC 29425, United States., Guo QJ; Department of Pathology & Laboratory Medicine, Medical University of South Carolina (MUSC), BEB407, Charleston, SC 29425, United States., Spruill LS; Department of Pathology & Laboratory Medicine, Medical University of South Carolina (MUSC), BEB407, Charleston, SC 29425, United States; Hollings Cancer Center, MUSC, United States., Lilly MB; Hollings Cancer Center, MUSC, United States; Department of Hematology/Oncology, MUSC, United States., Helke K; Department of Comparative Medicine, MUSC, United States., Li H; Hollings Cancer Center, MUSC, United States; Department of Public Health Sciences, MUSC, United States., Hanna GS; Department of Drug Discovery and Biomedical Sciences, MUSC, United States., Hamann MT; Department of Public Health Sciences, MUSC, United States; Department of Drug Discovery and Biomedical Sciences, MUSC, United States., Thomas C; Department of Biological & Physical Sciences, South Carolina State University, United States., Ahmed M; Department of Biological & Physical Sciences, South Carolina State University, United States., Gooz MB; Department of Drug Discovery and Biomedical Sciences, MUSC, United States., Findlay VJ; Department of Pathology & Laboratory Medicine, Medical University of South Carolina (MUSC), BEB407, Charleston, SC 29425, United States; Hollings Cancer Center, MUSC, United States., Turner DP; Department of Pathology & Laboratory Medicine, Medical University of South Carolina (MUSC), BEB407, Charleston, SC 29425, United States; Hollings Cancer Center, MUSC, United States. Electronic address: turnerda@musc.edu.
Jazyk:	angličtina
Zdroj:	Translational oncology [Transl Oncol] 2022 Mar; Vol. 17, pp. 101350. Date of Electronic Publication: 2022 Jan 25.
DOI:	10.1016/j.tranon.2022.101350
Abstrakt:	The molecular implications of food consumption on cancer etiology are poorly defined. The rate of nutrition associated non-enzymatic glycoxidation, a reaction that occurs between reactive carbonyl groups on linear sugars and nucleophilic amino, lysyl and arginyl groups on fats and proteins, is rapidly increased by food cooking and manufacturing processes. In this study, we assign nutrition-associated glycoxidation with significant oncogenic potential, promoting prostate tumor growth, progression, and metastasis in vivo. Advanced glycation end products (AGEs) are the final irreversible product of non-enzymatic glycoxidation. Exogenous treatment of prostate tumor cells with a single AGE peptide replicated glycoxidation induced tumor growth in vivo. Mechanistically, receptor for AGE (RAGE) deficiency in the stroma inhibited AGE mediated tumor growth. Functionally, AGE treatment induced RAGE dimerization in activated fibroblasts which sustained and increased the migratory potential of tumor epithelial cells. These data identify a novel nutrition associated pathway that can promote a tissue microenvironment conducive for aggressive tumor growth. Targeted and/or interventional strategies aimed at reducing AGE bioavailability as a consequence of nutrition may be viewed as novel chemoprevention initiatives. (Copyright © 2022. Published by Elsevier Inc.)
Databáze:	MEDLINE
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