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学科主题: 临床医学
题名:
Ca2+ channel subunit alpha 1D promotes proliferation and migration of endometrial cancer cells mediated by 17 beta-estradiol via the G protein-coupled estrogen receptor
作者: Hao, Juan1; Bao, Xiaoxia1; Jin, Bo3; Wang, Xiujuan3; Mao, Zebin3; Li, Xiaoping1; Wei, Lihui1; Shen, Danhua2; Wang, Jian-Liu1
关键词: calcium ; endometrial carcinoma ; Cav1.3 ; ERK1/2 ; rapid signaling effect
刊名: FASEB JOURNAL
发表日期: 2015-07-01
DOI: 10.1096/fj.14-265603
卷: 29, 期:7, 页:2883-2893
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology ; Biology ; Cell Biology
研究领域[WOS]: Biochemistry & Molecular Biology ; Life Sciences & Biomedicine - Other Topics ; Cell Biology
关键词[WOS]: ELEMENT-BINDING PROTEIN ; CALCIUM-CHANNELS ; RESPONSE ELEMENT ; PROSTATE-CANCER ; SIGNALING PATHWAY ; CARCINOMA-CELLS ; ACTIVATION ; MECHANISMS ; EXPRESSION ; MEMBRANE
英文摘要:

Calcium and calcium channels are closely related to the estrogen-induced nongenomic effect of endometrial carcinoma, but the specific role of calcium channels is unknown. This study aimed to explore the expression and the biologic effect of the L-type calcium channel in endometrial carcinoma cells and to clarify the molecular mechanism of the relationship between L-type calcium channels and estrogen. The immunohistochemical results showed that Ca2+ channel subunit alpha 1D (Cav1.3) expression was high in atypical hyperplasia (1.90 +/- 0.35) and endometrial carcinoma tissues (2.05 +/- 0.82) but weak (0.80 +/- 0.15) in benign endometrial tissues (P < 0.05). Treatment with 17 beta-estradiol rapidly increased Cav1.3 expression in a dose-and time-dependent manner, and 100 nM cell-impermeable beta-estradiol-6-(O-carboxymethyl) oxime: bovine serum albumin also promoted Cav1.3 expression. Transfection with small interfering RNA against G protein-coupled estrogen receptor (GPER) suppressed estrogen-induced up-regulation of Cav1.3 compared with control cells and markedly reduced the estrogen-induced phosphorylation of ERK1/2 and CREB. Knocking down the Cav1.3 significantly suppressed estrogen-stimulated Ca2+ influx, cell proliferation, and migration in endometrial cancer cells. Taken together, Cav1.3 was overexpressed in atypical hyperplasia and endometrial carcinoma, and the estrogen-induced phosphorylation of downstream molecular ERK1/2 and CREB is the result of activation of the GPER pathway. L-type channel Cav1.3 is required for estrogen-stimulated Ca2+ influx and contributes broadly to the development of endometrial cancer. The Cav1.3 channel may be a new target for endometrial carcinoma treatment.

语种: 英语
所属项目编号: 30973182 ; 81272869
项目资助者: National Natural Science Foundation of China
WOS记录号: WOS:000356859100018
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/59544
Appears in Collections:北京大学第二临床医学院_期刊论文

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作者单位: 1.Peking Univ, Peoples Hosp, Dept Obstet & Gynaecol, Beijing 100044, Peoples R China
2.Peking Univ, Peoples Hosp, Dept Pathol, Beijing 100044, Peoples R China
3.Peking Univ, Dept Biochem & Mol Biol, Beijing 100044, Peoples R China

Recommended Citation:
Hao, Juan,Bao, Xiaoxia,Jin, Bo,et al. Ca2+ channel subunit alpha 1D promotes proliferation and migration of endometrial cancer cells mediated by 17 beta-estradiol via the G protein-coupled estrogen receptor[J]. FASEB JOURNAL,2015,29(7):2883-2893.
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