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ER-alpha 36, a Variant of ER-alpha, Promotes Tamoxifen Agonist Action in Endometrial Cancer Cells via the MAPK/ERK and PI3K/Akt Pathways
Lin, Sheng-Li1,2; Yan, Li-Ying3; Zhang, Xin-Tian4; Yuan, Ju1,2; Li, Mo1,2; Qiao, Jie3; Wang, Zhao-Yi4; Sun, Qing-Yuan1,2
刊名PLOS ONE
2010-02-02
DOI10.1371/journal.pone.0009013
5期:2
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]HUMAN-BREAST-CANCER ; ACTIVATED PROTEIN-KINASE ; ESTROGEN-RECEPTOR-ALPHA ; SURGICAL ADJUVANT BREAST ; GROWTH-FACTOR ; ANTIESTROGEN RESISTANCE ; MOLECULAR-MECHANISMS ; C-MYC ; EXPRESSION ; ESTRADIOL
英文摘要

Background: Recently, a novel variant of ER-alpha, ER-alpha 36 was identified and cloned. ER-alpha 36 lacks intrinsic transcription activity and mainly mediates nongenomic estrogen signaling. Here, we studied the role of nongenomic estrogen signaling pathways mediated by ER-alpha 36 in tamoxifen resistance and agonist action.

Methodology: The cellular localization of ER-alpha 36 was examined by immunofluorescence in MCF-7 cells and Hec1A cells. MCF-7 breast cancer cells, MCF-7 cells expressing recombinant ER-alpha 36 (MCF-7/ER36), Hec1A endometrial cancer cells and Hec1A cells with siRNA knockdown of ER-alpha 36 (Hec1A/RNAiER36) were treated with 17 beta-estradial (E2) and tamoxifen (TAM) in the absence and presence of kinase inhibitor U0126 and LY294002. We examined phosphorylation of signaling molecules and the expression of c-Myc by immunoblotting, and tumor cell growth by MTT assay.

Conclusions: ER variant ER-alpha 36 enhances TAM agonist activity through activation of the membrane-initiated signaling pathways in endometrial cancer, and that ER-alpha 36 is involved in de novo and acquired TAM resistance in breast cancer.

语种英语
WOS记录号WOS:000274207200011
项目编号2006CB504004 ; 2006CB944005
资助机构National Basic Research Program of China
引用统计
被引频次:68[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/400002259/56159
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 Third Hosp, Dept Obstet & Gynecol, Ctr Reprod Med, Beijing 100871, Peoples R China
4.Creighton Univ, Sch Med, Dept Med Microbiol & Immunol, Omaha, NE USA
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Lin, Sheng-Li,Yan, Li-Ying,Zhang, Xin-Tian,et al. ER-alpha 36, a Variant of ER-alpha, Promotes Tamoxifen Agonist Action in Endometrial Cancer Cells via the MAPK/ERK and PI3K/Akt Pathways[J]. PLOS ONE,2010,5(2).
APA Lin, Sheng-Li.,Yan, Li-Ying.,Zhang, Xin-Tian.,Yuan, Ju.,Li, Mo.,...&Sun, Qing-Yuan.(2010).ER-alpha 36, a Variant of ER-alpha, Promotes Tamoxifen Agonist Action in Endometrial Cancer Cells via the MAPK/ERK and PI3K/Akt Pathways.PLOS ONE,5(2).
MLA Lin, Sheng-Li,et al."ER-alpha 36, a Variant of ER-alpha, Promotes Tamoxifen Agonist Action in Endometrial Cancer Cells via the MAPK/ERK and PI3K/Akt Pathways".PLOS ONE 5.2(2010).
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