Tumor Cell-educated Periprostatic Adipose Tissue Acquires an Aggressive Cancer-promoting Secretory Profile

• Type: Article in International Scientific Journal
• Date: 2012

Authors

Ricardo J T Ribeiro (Author) Other; Catia P D Monteiro (Author) Other; Virginia F P M Cunha (Author) Other; Azevedo, ASM (Author) Other; Maria J Oliveira (Author) FEUP; Rosario Monteiro (Author) FMUP; Avelino M Fraga (Author) Other; Paulo Principe (Author) Other; Carlos Lobato (Author) Other; Francisco Lobo (Author) Other; Antonio Morais (Author) Other; Vitor Silva (Author) Other; Jose Sanches Magalhaes (Author) Other; Jorge Oliveira (Author) Other; Joao T Guimaraes (Author) FMUP; Carlos M S Lopes (Author) Other; Rui M Medeiros (Author) ICBAS

Journal

Title: Cellular Physiology and Biochemistry

Vol. 29

Pages: 233-240

ISSN: 1015-8987

Publisher: Cell Physiol Biochem Press

Indexing

ISI Web of Knowledge - 60 Citations

Scopus - 66 Citations

Scientific classification

FOS: Medical and Health sciences > Basic medicine

Other information

Authenticus ID: P-002-GX3

DOI: 10.1159/000337604

Abstract (EN): Background/Aims: The microenvironment produces important factors that are crucial to prostate cancer (PCa) progression. However, the extent to which the cancer cells stimulate periprostatic adipose tissue (PPAT) to produce these proteins is largely unknown. Our purpose was to determine whether PCa cell-derived factors influence PPAT metabolic activity. Methods: Primary cultures of human PPAT samples from PCa patients (adipose tissue organotypic explants and primary stromal vascular fraction, SVF) were stimulated with conditioned medium (CM) collected from prostate carcinoma (PC3) cells. Cultures without CM were used as control. We used multiplex analysis and ELISA for protein quantification, qPCR to determine mitochondrial DNA (mtDNA) copy number and zymography for matrix metalloproteinase activity, in order to evaluate the response of adipose tissue explants and SVFs to PC3 CM. Results: Stimulation of PPAT explants with PCa PC3 CM induced adipokines associated with cancer progression (osteopontin, tumoral necrosis factor alpha and interleukin-6) and reduced the expression of the protective adipokine adiponectin. Notably, osteopontin protein expression was 13-fold upregulated. Matrix metalloproteinase 9 activity and mitochondrial DNA copy number were higher after stimulation with cancer CM. Stromovascular cells from PPAT in culture were not influenced by tumor-derived factors. Conclusion: The modulation of adipokine expression by tumor CM indicates the pervasive extent to which tumor cells command PPAT to produce factors favorable to their aggressiveness. Copyright (C) 2012 S. Karger AG, Basel

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 8