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A novel variant of ER-alpha, ER-alpha36 mediates testosterone-stimulated ERK and Akt activation in endometrial cancer Hec1A cells
Lin, Sheng-Li1,2; Yan, Li-Ying3; Liang, Xing-Wei1; Wang, Zhen-Bo1,2; Wang, Zhao-Yi4; Qiao, Jie3; Schatten, Heide5; Sun, Qing-Yuan1
刊名REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY
2009-09-24
DOI10.1186/1477-7827-7-102
7
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Endocrinology & Metabolism ; Reproductive Biology
资助者National Basic Research Program of China ; National Basic Research Program of China
研究领域[WOS]Endocrinology & Metabolism ; Reproductive Biology
关键词[WOS]POLYCYSTIC-OVARY-SYNDROME ; ESTROGEN-RECEPTOR-ALPHA ; EPIDERMAL-GROWTH-FACTOR ; HUMAN BREAST-CANCER ; AROMATASE EXPRESSION ; PROTEIN-KINASE ; CARCINOMA ; ENDOCRINE ; PATHWAYS ; THERAPY
英文摘要

Background: Endometrial cancer is one of the most common gynecologic malignancies and its incidence has recently increased. Experimental and epidemiological data support that testosterone plays an important role in the pathogenesis of endometrial cancer, but the underlying mechanism has not been fully understood. Recently, we identified and cloned a variant of estrogen receptor (ER) alpha, ER-alpha36. The aim of the present study was to investigate the role of ER-alpha36 in testosterone carcinogenesis.

Methods: The cellular localization of ER-alpha36 was determined by immunofluorescence. Hec1A endometrial cancer cells (Hec1A/V) and Hec1A cells with siRNA knockdown of ER-alpha36 (Hec1A/RNAi) were treated with testosterone, ERK and Akt phosphorylation was assessed by Western blot analysis. Furthermore, the kinase inhibitors U0126 and LY294002 and the aromatase inhibitor letrozole were used to elucidate the pathway underlying testosterone-induced activities.

Results: Immunofluorescence shows that ER-alpha36 was localized on the plasma membrane of the both ER-alpha-and androgen receptor-negative endometrial cancer Hec1A cells. Testosterone induced ERK and Akt phosphorylation, which could be abrogated by ER-alpha 36 shRNA knockdown or the kinase inhibitors, U0126 and LY294002, and the aromatase inhibitor letrozole.

Conclusion: Testosterone induces ERK and Akt phosphorylation via the membrane-initiated signaling pathways mediated by ER-alpha36, suggesting a possible involvement of ER-alpha 36 in testosterone carcinogenesis.

语种英语
所属项目编号2006CB504004 ; 2006CB944005
资助者National Basic Research Program of China ; National Basic Research Program of China
WOS记录号WOS:000270995000001
引用统计
被引频次:42[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/400002259/54383
专题北京大学第三临床医学院_生殖医学中心
作者单位1.Chinese Acad Sci, Grad Sch, Beijing, Peoples R China
2.Chinese Acad Sci, Inst Zool, State Key Lab Reprod Biol, Beijing, Peoples R China
3.Peking Univ, Hosp 3, Dept Obstet & Gynecol, Ctr Reprod Med, Beijing 100871, Peoples R China
4.Creighton Univ, Sch Med, Dept Med Microbiol & Immunol, Omaha, NE USA
5.Univ Missouri, Dept Vet Pathobiol, Columbia, MO 65211 USA
推荐引用方式
GB/T 7714
Lin, Sheng-Li,Yan, Li-Ying,Liang, Xing-Wei,et al. A novel variant of ER-alpha, ER-alpha36 mediates testosterone-stimulated ERK and Akt activation in endometrial cancer Hec1A cells[J]. REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY,2009,7.
APA Lin, Sheng-Li.,Yan, Li-Ying.,Liang, Xing-Wei.,Wang, Zhen-Bo.,Wang, Zhao-Yi.,...&Sun, Qing-Yuan.(2009).A novel variant of ER-alpha, ER-alpha36 mediates testosterone-stimulated ERK and Akt activation in endometrial cancer Hec1A cells.REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY,7.
MLA Lin, Sheng-Li,et al."A novel variant of ER-alpha, ER-alpha36 mediates testosterone-stimulated ERK and Akt activation in endometrial cancer Hec1A cells".REPRODUCTIVE BIOLOGY AND ENDOCRINOLOGY 7(2009).
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