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STAMP2是人类脂肪来源干细胞分化和脂肪细胞促进前列腺癌生长所必需的。

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

作者信息

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

机构信息

Department of Biosciences, University of Oslo, Oslo, Norway.

Department of Cancer Genetics and Informatics, Oslo University Hospital, Oslo, Norway.

出版信息

Oncotarget. 2016 Aug 9;8(54):91817-91827. doi: 10.18632/oncotarget.11131. eCollection 2017 Nov 3.

DOI:10.18632/oncotarget.11131
PMID:29190878
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5696144/
Abstract

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 .

摘要

前列腺六次跨膜蛋白2(STAMP2)与前列腺癌(PCa)和代谢疾病均有关联。STAMP2在小鼠脂肪组织中具有独特的抗炎和促代谢特性,但关于其在人类代谢组织中的作用的信息有限。利用人脂肪来源干细胞(ASC),我们发现STAMP2在脂肪生成过程中表达显著上调。在ASC中,shRNA介导的STAMP2敲低显著抑制脂肪生成,并干扰脂肪生成基因的最佳表达和脂肪细胞代谢功能。此外,在ASC脂肪细胞中敲低STAMP2后,ASC来源的脂肪细胞介导的裸鼠前列腺肿瘤生长刺激作用显著降低。这些结果表明,STAMP2对于ASC正常转化为脂肪细胞及其代谢功能,以及促进PCa生长的能力至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3584/5696144/8fed07da514c/oncotarget-08-91817-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3584/5696144/03d5ad4f6af7/oncotarget-08-91817-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3584/5696144/0809c4c9e5c8/oncotarget-08-91817-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3584/5696144/d4beea2cda66/oncotarget-08-91817-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3584/5696144/8fed07da514c/oncotarget-08-91817-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3584/5696144/03d5ad4f6af7/oncotarget-08-91817-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3584/5696144/0809c4c9e5c8/oncotarget-08-91817-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3584/5696144/d4beea2cda66/oncotarget-08-91817-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3584/5696144/8fed07da514c/oncotarget-08-91817-g004.jpg

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