ELL is an HIF-1 alpha Partner That Regulates and Responds to Hypoxia Response in PC3 Cells
文献类型：期刊论文
| 作者 | Liu, Lingqi1,2,3; Ai, Junkui3; Xiao, Wuhan4; Liu, June3; Wang, Yujuan5; Xin, Dianqi1,2; He, Zhisong1,2; Guo, Yinglu1,2; Wang, Zhou3,6,7 |
| 刊名 | PROSTATE
 |
| 出版日期 | 2010-05-15 |
| 卷号 | 70期号:7页码:797-805 |
| 关键词 | ELL hypoxia HIF-1 alpha prostate cancer |
| ISSN号 | 0270-4137 |
| 通讯作者 | He, ZS, Peking Univ, Hosp 1, Dept Urol, 8 Xishiku St, Beijing 100034, Peoples R China |
| 中文摘要 | BACKGROUND. Eleven nineteen lysine-rich leukemia (ELL) plays an important role in tumorigenesis and animal development. HIF-1 is a transcriptional factor that functions as a master regulator of O-2 homeostasis. Our previous studies showed that a binding partner of ELL, U19/Eaf2, can modulate HIF-1 alpha activity and hypoxia response, suggesting that ELL may also influence HIF-1 alpha pathway and hypoxia response. METHODS. Co-localization and co-immunoprecipitation were performed to test the interaction between ELL and HIF-1 alpha. PC3 cells with stable ELL knockdown and PC3 cells with stable ELL overexpression, along with their controls, were established using lentiviral expression system. Western blot and real-time PCR were performed to test the effect of ELL on HIF-1 alpha protein and its down-stream gene transcription. To elucidate potential effect of hypoxia on ELL, cell growth and colony formation assays were performed using PC3 subline with stable ELL overexpression. RESULTS. ELL is associated with HIF-1 alpha in transfected cells. In PC3 prostate cancer cells, ELL inhibited HIF-1 alpha protein level and down-stream gene expression. As expected, ELL inhibited cell growth and colony formation under normoxia. Interestingly, the inhibition was alleviated under hypoxia. CONCLUSIONS. Our findings suggest that ELL and HIF-1 alpha are binding partners and can modulate the functions of each other in hypoxia. Prostate 70: 797-805, 2010. (C) 2010 Wiley-Liss, Inc. |
| 英文摘要 | BACKGROUND. Eleven nineteen lysine-rich leukemia (ELL) plays an important role in tumorigenesis and animal development. HIF-1 is a transcriptional factor that functions as a master regulator of O(2) homeostasis. Our previous studies showed that a binding partner of ELL, U19/Eaf2, can modulate HIF-1 alpha activity and hypoxia response, suggesting that ELL may also influence HIF-1 alpha pathway and hypoxia response. |
| WOS标题词 | Science & Technology ; Life Sciences & Biomedicine |
| 学科主题 | Endocrinology & Metabolism; Urology & Nephrology |
| 类目[WOS] | Endocrinology & Metabolism ; Urology & Nephrology |
| 研究领域[WOS] | Endocrinology & Metabolism ; Urology & Nephrology |
| 关键词[WOS] | ELONGATION-FACTOR ELL ; TUMOR-SUPPRESSOR PROTEIN ; PROSTATE-CANCER ; INDUCIBLE FACTOR-1 ; MYELOID-LEUKEMIA ; GROWTH ; POLYMERASE ; HIF-1 ; GENE ; T(11-19)(Q23-P13.1) |
| 收录类别 | SCI |
| 资助信息 | NIH [R37 DK51193, R01 CA120386, P50 CA90386] |
| 语种 | 英语 |
| WOS记录号 | WOS:000277338800012 |
| 公开日期 | 2010-12-23 |
| 源URL | [http://ir.ihb.ac.cn/handle/342005/13749]  |
| 专题 | 水生生物研究所_水生生物分子与细胞生物学研究中心_期刊论文 |
| 作者单位 | 1.Peking Univ, Hosp 1, Dept Urol, Beijing 100034, Peoples R China 2.Peking Univ, Inst Urol, Beijing 100034, Peoples R China 3.Univ Pittsburgh, Sch Med, Dept Urol, Pittsburgh, PA 15232 USA 4.Chinese Acad Sci, Inst Hydrobiol, Wuhan, Peoples R China 5.Univ Pittsburgh, Sch Med, Dept Pathol, Pittsburgh, PA 15232 USA 6.Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Pittsburgh, PA 15232 USA 7.Univ Pittsburgh, Sch Med, Inst Canc, Pittsburgh, PA 15232 USA |
| 推荐引用方式 GB/T 7714 | Liu, Lingqi,Ai, Junkui,Xiao, Wuhan,et al. ELL is an HIF-1 alpha Partner That Regulates and Responds to Hypoxia Response in PC3 Cells[J]. PROSTATE,2010,70(7):797-805. |
| APA | Liu, Lingqi.,Ai, Junkui.,Xiao, Wuhan.,Liu, June.,Wang, Yujuan.,...&Wang, Zhou.(2010).ELL is an HIF-1 alpha Partner That Regulates and Responds to Hypoxia Response in PC3 Cells.PROSTATE,70(7),797-805. |
| MLA | Liu, Lingqi,et al."ELL is an HIF-1 alpha Partner That Regulates and Responds to Hypoxia Response in PC3 Cells".PROSTATE 70.7(2010):797-805. |
入库方式： OAI收割
来源：水生生物研究所
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