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学科主题临床医学
Targeting Androgen Receptor to Suppress Macrophage-induced EMT and Benign Prostatic Hyperplasia (BPH) Development
Lu, Tianjing1,2,3,5; Lin, Wen-Jye1,2,3; Izumi, Kouji1,2,3; Wang, Xiaohai1,2,3; Xu, Defeng1,2,3; Fang, Lei-Ya1,2,3; Li, Lei1,2,3; Jiang, Qi1,2,3; Jin, Jie5; Chang, Chawnshang1,2,3,6
刊名MOLECULAR ENDOCRINOLOGY
2012-10-01
DOI10.1210/me.2012-1079
26期:10页:1707-1715
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Endocrinology & Metabolism
研究领域[WOS]Endocrinology & Metabolism
关键词[WOS]EPITHELIAL-MESENCHYMAL TRANSITION ; DEPRIVATION THERAPY ; MICE LACKING ; CANCER ; DIFFERENTIATION ; CELLS ; PROLIFERATION ; MORPHOGENESIS ; INFLAMMATION ; PROGRESSION
英文摘要

Early studies suggested macrophages might play roles in inflammation-associated benign prostatic hyperplasia (BPH) development, yet the underlying mechanisms remain unclear. Here we first showed that CD68(+) macrophages were identified in both epithelium and the stromal area of human BPH tissues. We then established an in vitro co-culture model with prostate epithelial and macrophage cell lines to study the potential impacts of infiltrating macrophages in the BPH development and found that co-culturing prostate epithelial cells with macrophages promoted migration of macrophages. In a three-dimensional culture system, the sphere diameter of BPH-1 prostate cells was significantly increased during coculture with THP-1 macrophage cells. Mechanism dissection suggested that expression levels of epithelial-mesenchymal transition (EMT) markers, such as N-cadherin, Snail, and TGF-beta 2, were increased, and administration of anti-TGF-beta 2 neutralizing antibody during co-culture suppressed the EMT and THP-1-mediated growth of BPH-1 cells, suggesting THP-1 might go through EMT to influence the BPH development and progression. Importantly, we found that modulation of androgen receptor (AR) in BPH-1 and mPrE cells significantly increased THP-1 and RAW264.7 cell migration, respectively, and enhanced expression levels of EMT markers, suggesting that AR in prostate epithelial cells might play a role in promoting macrophage-mediated EMT in prostate epithelial cells. Silencing AR function via an AR degradation enhancer, ASC-J9, decreased the macrophage migration to BPH-1 cells and suppressed EMT marker expression. Together, these results provide the first evidence to demonstrate that prostate epithelial AR function is important for macrophage-mediated EMT and proliferation of prostate epithelial cells, which represents a previously unrecognized role of AR in the cross-talk between macrophages and prostate epithelial cells. These results may provide new insights for a new therapeutic approach to battle BPH via targeting AR and AR-mediated inflammatory signaling pathways. (Molecular Endocrinology 26: 1707-1715, 2012)

语种英语
WOS记录号WOS:000309509500008
项目编号CA127300 ; CA156700 ; W81XWH-10-1-0300 ; DOH99-TD-B-111-004 ; 2012CB518305
资助机构National Institutes of Health ; Department of Defense ; Taiwan Department of Health Clinical Trial and Research Center of Excellence ; China 973 National Program on Key Basic Research Project
引用统计
被引频次:31[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/67097
专题北京大学第一临床医学院_泌尿外科
作者单位1.Univ Rochester, Med Ctr, George Whipple Lab Canc Res, Dept Pathol, Rochester, NY 14642 USA
2.Univ Rochester, Med Ctr, George Whipple Lab Canc Res, Dept Urol, Rochester, NY 14642 USA
3.Univ Rochester, Med Ctr, George Whipple Lab Canc Res, Dept Radiat Oncol, Rochester, NY 14642 USA
4.Univ Rochester, Med Ctr, Wilmot Canc Ctr, Rochester, NY 14642 USA
5.China Med Univ Hosp, Sex Hormone Res Ctr, Taichung 404, Taiwan
6.Peking Univ, Hosp 1, Inst Urol, Beijing 100034, Peoples R China
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GB/T 7714
Lu, Tianjing,Lin, Wen-Jye,Izumi, Kouji,et al. Targeting Androgen Receptor to Suppress Macrophage-induced EMT and Benign Prostatic Hyperplasia (BPH) Development[J]. MOLECULAR ENDOCRINOLOGY,2012,26(10):1707-1715.
APA Lu, Tianjing.,Lin, Wen-Jye.,Izumi, Kouji.,Wang, Xiaohai.,Xu, Defeng.,...&Chang, Chawnshang.(2012).Targeting Androgen Receptor to Suppress Macrophage-induced EMT and Benign Prostatic Hyperplasia (BPH) Development.MOLECULAR ENDOCRINOLOGY,26(10),1707-1715.
MLA Lu, Tianjing,et al."Targeting Androgen Receptor to Suppress Macrophage-induced EMT and Benign Prostatic Hyperplasia (BPH) Development".MOLECULAR ENDOCRINOLOGY 26.10(2012):1707-1715.
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