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学科主题: 基础医学
题名:
Hypoxia-induced Up-regulation of Aquaporin-1 Protein in Prostate Cancer Cells in a p38-dependent Manner
作者: Tie, Lu1,2; Lu, Ning1,2; Pan, Xue-Yang1,2; Pan, Yan1,2; An, Yu1,2; Gao, Jun-Wei1,2; Lin, Yan-Hua1,2; Yu, He-Ming3; Li, Xue-Jun1,2
关键词: Aquaporin-1 (AQP1) ; Hypoxia ; p38 ; MAPK ; PKC ; Calcium ; Cancer cells
刊名: CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
发表日期: 2012
DOI: 10.1159/000337608
卷: 29, 期:1-2, 页:269-280
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cell Biology ; Physiology
研究领域[WOS]: Cell Biology ; Physiology
关键词[WOS]: WATER CHANNELS ; INDUCIBLE FACTOR-1 ; KINASE-C ; PHOSPHATIDYLINOSITOL 3&prime ; -KINASE ; INDUCED PROLIFERATION ; SIGNALING PATHWAYS ; AQP1 EXPRESSION ; BRAIN-TUMORS ; GENE ; ACTIVATION
英文摘要:

Background/Aims: Aquaporin-1 (AQP1) is a glycoprotein that mediates osmotic water transport, its expression has been found to correlate with tumour stage in some tumours. However, the mechanism by which AQP1 protein expression is regulated in tumor cells remains to be fully elucidated. We hypothesized that hypoxia might play an important role in AQP1 induction during tumorigenesis and at the late stages of tumor development. Methods: Isotonic and serum-free hypoxic models were used to investigate AQP1 expression in PC-3M human prostate cancer cells. Results: AQP1 expression was up-regulated by density-induced pericellular hypoxia and cobalt(II) chloride (CoCl 2)-induced hypoxia at the transcriptional level. Moreover, phosphorylation of p38 mitogen-activated protein kinase (MAPK) was induced by density-induced pericellular hypoxia and CoCl 2 induced hypoxia, specific inhibitors of p38 MAPK could concentration-dependently block those effects of hypoxia on AQP1 expression. Intracellular calcium ion (Ca2+) and protein kinase C (PKC) were shown to be responsible for the activation of p38 MAPK pathway. In addition, AQP1 induction in dense cultures was dependent on lowered oxygen (O-2) tension. In high cell density culture, certain secretory proteins might induce AQP1 expression indirectly. Conclusion: These findings suggest that AQP1 could be induced by hypoxia at transcription level, and the regulation of AQP1 in PC-3M cells is dependent on calcium, PKC and p38 MAPK, as well as low oxygen tension. Copyright (C) 2012 S. Karger AG, Basel

语种: 英语
所属项目编号: 30901803 ; 91129727 ; 81020108031 ; 30973558 ; 30572202 ; 30901815 ; 20090001120046 ; 2009ZX09103-144 ; B07001
项目资助者: National Natural Science Foundation of China ; Research Fund for the Doctoral Program of Higher Education of China ; Ministry of Science and Technology in China ; Ministry of Education of China
WOS记录号: WOS:000301141400028
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/55753
Appears in Collections:基础医学院_药理学系_期刊论文

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作者单位: 1.Peking Univ, Inst Syst Biomed, Beijing 100191, Peoples R China
2.Peking Univ, Dept Pharmacol, Sch Basic Med Sci, State Key Lab Nat & Biomimet Drugs, Beijing 100191, Peoples R China
3.Natl Res Inst Family Planning, Beijing, Peoples R China

Recommended Citation:
Tie, Lu,Lu, Ning,Pan, Xue-Yang,et al. Hypoxia-induced Up-regulation of Aquaporin-1 Protein in Prostate Cancer Cells in a p38-dependent Manner[J]. CELLULAR PHYSIOLOGY AND BIOCHEMISTRY,2012,29(1-2):269-280.
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