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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
卷号	7页码:8
ISSN号	1477-7827
DOI	10.1186/1477-7827-7-102
通讯作者	Sun, qing-yuan(sunqy@ioz.ac.cn)
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.
WOS关键词	POLYCYSTIC-OVARY-SYNDROME ; ESTROGEN-RECEPTOR-ALPHA ; EPIDERMAL-GROWTH-FACTOR ; HUMAN BREAST-CANCER ; AROMATASE EXPRESSION ; PROTEIN-KINASE ; CARCINOMA ; ENDOCRINE ; PATHWAYS ; THERAPY
WOS研究方向	Endocrinology & Metabolism ; Reproductive Biology
WOS类目	Endocrinology & Metabolism ; Reproductive Biology
语种	英语
出版者	BIOMED CENTRAL LTD
WOS记录号	WOS:000270995000001
内容类型	期刊论文
URI标识	http://www.corc.org.cn/handle/1471x/2395200
专题	中国科学院大学
通讯作者	Sun, Qing-Yuan
作者单位	1.Chinese Acad Sci, Inst Zool, State Key Lab Reprod Biol, Beijing, Peoples R China 2.Chinese Acad Sci, Grad Sch, 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,2009,7:8.
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,7,8.
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):8.

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