Research Papers:

STAMP2 is required for human adipose-derived stem cell differentiation and adipocyte-facilitated prostate cancer growth in vivo

Torstein Lindstad, Su Qu, Jørgen Sikkeland, Yang Jin, Alexandr Kristian, Gunhild M. Mælandsmo, Philippe Collas and Fahri Saatcioglu _

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Oncotarget. 2017; 8:91817-91827. https://doi.org/10.18632/oncotarget.11131

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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

Correspondence to:

Fahri Saatcioglu, email: [email protected]

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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