STAMP2 is required for human adipose-derived stem cell differentiation and adipocyte-facilitated prostate cancer growth in vivo
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Torstein Lindstad1, Su Qu1, Jørgen Sikkeland1,2, Yang Jin1,2, Alexandr Kristian3, Gunhild M. Mælandsmo3, Philippe Collas4 and Fahri Saatcioglu1,2
1Department of Biosciences, University of Oslo, Oslo, Norway
2Department of Cancer Genetics and Informatics, Oslo University Hospital, Oslo, Norway
3Department of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway
4Institute of Basic Medical Sciences, Norwegian Center for Stem Cell Research, University of Oslo, Oslo, Norway
Fahri Saatcioglu, email: email@example.com
Keywords: STAMP2, ASC, lipogenesis, adipogenesis, prostate cancer
Received: May 24, 2016 Accepted: July 01, 2016 Published: August 09, 2016
Six Transmembrane Protein of Prostate 2 (STAMP2) has been implicated in both prostate cancer (PCa) and metabolic disease. STAMP2 has unique anti-inflammatory and pro-metabolic properties in mouse adipose tissue, but there is limited information on its role in human metabolic tissues. Using human adipose-derived stem cells (ASCs), we report that STAMP2 expression is dramatically upregulated during adipogenesis. shRNA-mediated STAMP2 knockdown in ASCs significantly suppresses adipogenesis and interferes with optimal expression of adipogenic genes and adipocyte metabolic function. Furthermore, ASC-derived adipocyte-mediated stimulation of prostate tumor growth in nude mice is significantly reduced upon STAMP2 knockdown in ASC adipocytes. These results suggest that STAMP2 is crucial for normal ASC conversion into adipocytes and their metabolic function, as well as their ability to facilitate PCa growth in vivo.
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