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      Ca2+ channel subunit α 1D promotes proliferation and migration of endometrial cancer cells mediated by 17β-estradiol via the G protein-coupled estrogen receptor.

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          Abstract

          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 Ca(2+) channel subunit α 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 17β-estradiol rapidly increased Cav1.3 expression in a dose- and time-dependent manner, and 100 nM cell-impermeable β-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 Ca(2+) 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 Ca(2+) influx and contributes broadly to the development of endometrial cancer. The Cav1.3 channel may be a new target for endometrial carcinoma treatment.

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          Author and article information

          Journal
          FASEB J.
          FASEB journal : official publication of the Federation of American Societies for Experimental Biology
          1530-6860
          0892-6638
          Jul 2015
          : 29
          : 7
          Affiliations
          [1 ] *Department of Obstetrics and Gynaecology and Department of Pathology, Peking University People's Hospital, Beijing, China; and Department of Biochemistry and Molecular Biology, Peking University, Beijing, China.
          [2 ] *Department of Obstetrics and Gynaecology and Department of Pathology, Peking University People's Hospital, Beijing, China; and Department of Biochemistry and Molecular Biology, Peking University, Beijing, China wangjianliu@pkuph.edu.cn.
          Article
          fj.14-265603
          10.1096/fj.14-265603
          25805831
          fa3a0037-bfaa-49ec-a44c-3e22442595e1
          © FASEB.
          History

          Cav1.3,ERK1/2,calcium,endometrial carcinoma,rapid signaling effect

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