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学科主题临床医学
Evidence of TGF-beta 1 mediated epithelial-mesenchymal transition in immortalized benign prostatic hyperplasia cells
Hu, Shuai1,2,3; Yu, Wei1,2,3; Lv, Tian-Jing1,2,3; Chang, Chawn-Shang4,5; Li, Xin1,2,3; Jin, Jie1,2,3
关键词Benign Prostate Hyperplasia Epithelial-mesenchymal Transition
刊名MOLECULAR MEMBRANE BIOLOGY
2014-03-01
DOI10.3109/09687688.2014.894211
31期:2-3页:103-110
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Cell Biology
研究领域[WOS]Biochemistry & Molecular Biology ; Cell Biology
关键词[WOS]TGF-BETA ; CANCER ; DIFFERENTIATION ; ANDROGEN ; INVASION ; WPMY-1
英文摘要

Expression of epithelial-mesenchymal transition (EMT) markers has been detected clinically in benign prostatic hyperplasia (BPH) tissues. To understand the molecular basis, we investigated the role of stromal microenvironment in the progression of EMT in BPH cells. First, we used cell culture supernatant from normal prostate stromal WPMY-1 cells to provide supernatant-conditioned medium (WSCM) to culture the BPH-1 cell line. Then, the morphological changes and migratory capacity were detected in BPH-1 cells. The expression of EMT markers was examined in BPH-1 cells by Western blot and immunofluorescent analysis. Finally, to investigate the role of transforming growth factor beta 1 (TGF-beta 1) in this process, the WSCM-cultured cells were treated with monoclonal antibody against TGF-beta 1 to study its effect on EMT. We found that the morphology of BPH-1 cells changed to a spindle-like shape after cultured in WSCM, and the levels of E-cadherin and cytokeratin 5/8 (CK5/8) were significantly lower than the cells cultured in ordinary medium. These BPH-1 cells were also tested positive for mesenchymal markers vimentin and a-smooth muscle actin (SMA) as well as Snail. We also found WSCM can increase the migratory capacity of BPH-1 cells. In addition, when they were treated with anti-TGF-beta 1, upregulation of E-cadherin and CK5/8 levels was observed but no expression of vimentin, alpha-SMA or Snail was detected. Furthermore, phosphorylated-Smad3 expression in WSCM-cultured BPH-1 cells was also suppressed by anti-TGF-beta 1 treatment. Our results demonstrated that stromal cell supernatant was able to induce EMT in BPH-1 cells, possibly through secreting TGF-beta 1 to activate Smad signaling. Our results suggest novel molecular targets for clinical treatment of BPH by modification of stromal microenvironment through inhibiting TGF-beta 1/Smad expression.

语种英语
WOS记录号WOS:000335340200005
引用统计
被引频次:7[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/400002259/55370
专题北京大学第一临床医学院_泌尿外科
作者单位1.Peking Univ, Dept Urol, Hosp 1, Beijing 100871, Peoples R China
2.Peking Univ, Inst Urol, Beijing 100871, Peoples R China
3.Natl Res Ctr Genitourinary Oncol, Beijing, Peoples R China
4.Univ Rochester, Med Ctr, Dept Pathol, George Whipple Lab Canc Res,Dept Urol,Dept Radiat, Rochester, NY 14642 USA
5.Univ Rochester, Med Ctr, Wilmot Canc Ctr, Rochester, NY 14642 USA
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GB/T 7714
Hu, Shuai,Yu, Wei,Lv, Tian-Jing,et al. Evidence of TGF-beta 1 mediated epithelial-mesenchymal transition in immortalized benign prostatic hyperplasia cells[J]. MOLECULAR MEMBRANE BIOLOGY,2014,31(2-3):103-110.
APA Hu, Shuai,Yu, Wei,Lv, Tian-Jing,Chang, Chawn-Shang,Li, Xin,&Jin, Jie.(2014).Evidence of TGF-beta 1 mediated epithelial-mesenchymal transition in immortalized benign prostatic hyperplasia cells.MOLECULAR MEMBRANE BIOLOGY,31(2-3),103-110.
MLA Hu, Shuai,et al."Evidence of TGF-beta 1 mediated epithelial-mesenchymal transition in immortalized benign prostatic hyperplasia cells".MOLECULAR MEMBRANE BIOLOGY 31.2-3(2014):103-110.
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