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学科主题: 临床医学
题名:
CTRP3 Stimulates Proliferation and Anti-Apoptosis of Prostate Cells through PKC Signaling Pathways
作者: Hou, Qi1; Lin, Jinyan2; Huang, Wentao3; Li, Maoyin3; Feng, Jianhua1; Mao, Xiangming4
刊名: PLOS ONE
发表日期: 2015-07-28
DOI: 10.1371/journal.pone.0134006
卷: 10, 期:7
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Multidisciplinary Sciences
研究领域[WOS]: Science & Technology - Other Topics
关键词[WOS]: C1Q/TNF-RELATED PROTEIN-3 CTRP3 ; PROMOTES PROLIFERATION ; ADIPOSE-TISSUE ; CTRP3/CARTDUCIN ; PARALOG ; METABOLISM ; EXPRESSION ; CARTDUCIN ; ADIPOKINE ; CORS-26
英文摘要:

C1q/TNF-related protein-3 (CTRP3) is a novel adipokine with roles in multiple cellular processes. However, little is known about its function in prostate cells. This study investigated the effects and mechanisms of CTRP3 in prostate cells. We first generated and purified CTRP3 protein in HEK 293T cells. Proliferation of RWPE-1 prostate cells was evaluated by MTT analyses under treatment with different concentrations of CTRP3 for various exposure times. The results revealed maximum enhancement of proliferation with 10 mu g/mL CTRP3 for 72 h. Cell apoptosis and cell cycle were determined by TUNEL staining and flow cytometry analysis. TUNEL assay showed decreased TUNEL-positive cells in RWPE-1 prostate cells treated with CTRP3, and flow cytometry showed significantly decreased apoptotic cells upon CTRP3 treatment (treated cells, 8.34 +/- 1.175 vs. controls, 20.163 +/- 0.35) (P < 0.01). Moreover, flow cytometry analysis also showed a significant decrease of cells in the G1 phase and an increase of cells in the S and G2 phase upon CTRP3 treatment (treated cells, 42.85 +/- 1.40 vs. control, 52.77 +/- 0.90; 28.41 +/- 0.57 vs. 23.49 +/- 1.13; 27.08 +/- 1.97 vs. 22.20 +/- 1.32, respectively) (all P < 0.05). Two-dimensional gel electrophoresis and mass spectrometry identified differentially expressed proteins, including cytokeratin-19, GLRX3 and DDAH1, which were upregulated in CTRP3 treated cells, and cytokeratin-17 and 14-3-3 sigma, which were downregulated. GLRX3, DDAH1 and 14-3-3 sigma were confirmed using western blot analysis. A PKC inhibitor, staurosporine, was used to inhibit PKC activity in CTRP3 treated RWPE-1 cells. Staurosporine completely abolished the CTRP3-induced increased phosphorylation of intracellular PKC substrates and CTRP3-stimulated effect by RWPE-1 cells. Our results provide the first evidence for a physiological role of the novel adipokine, CTRP3, in prostate cells. Our findings suggest that CTRP3 could improve proliferation and anti-apoptosis of prostate cells through protein kinase C signaling pathways.

语种: 英语
所属项目编号: 201406093001004
项目资助者: Medical Science and Technology Program of Shenzhen Longgang district
WOS记录号: WOS:000358595900063
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/51365
Appears in Collections:北京大学深圳医院_泌尿外科_期刊论文

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作者单位: 1.Longgang Dist Cent Hosp, Dept Urol, Shenzhen, Peoples R China
2.Peking Univ, Shenzhen Hosp, Dept Urol, Shenzhen, Peoples R China
3.Southern Med Univ, Nanfang Hosp, Hlth management Ctr, Guangzhou, Guangdong, Peoples R China
4.Sun Yat Sen Univ, Affiliated Hosp 3, Dept Urol, Guangzhou 510275, Guangdong, Peoples R China

Recommended Citation:
Hou, Qi,Lin, Jinyan,Huang, Wentao,et al. CTRP3 Stimulates Proliferation and Anti-Apoptosis of Prostate Cells through PKC Signaling Pathways[J]. PLOS ONE,2015,10(7).
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