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Activation of membrane estrogen receptor: MAPK signaling by cadmium chloride and sodium arsenite in human lung adenocarcinoma cells
Author(s) -
Hyzer Jeffrey M.,
Krauss Katazyna A.,
Black Austin T.,
Todd Sarah L.,
Elpers Julia T.,
Hoerter Jacob E.,
Klinge Carolyn M.,
Huff Mary O.
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.644.7
Subject(s) - estrogen receptor , gper , chemistry , phosphorylation , mapk/erk pathway , endocrinology , medicine , cadmium chloride , biology , cadmium , biochemistry , cancer , organic chemistry , breast cancer
Estrogens have been implicated in non‐small cell lung cancer (NSCLC) risk but the contribution and possible mechanisms of the endocrine disruptors, cadmium chloride (CdCl 2 ) and sodium arsenate (NaAsO 2 ), have not been delineated. In this study, cell proliferation of NCI‐H1793 human lung adenocarcinoma cells increased following treatment with nanomolar concentrations of CdCl 2 and NaAsO 2 , and like 17β‐estadiol (E 2 ), 10 min treatment stimulated phosphorylation of ERK1/2. In the presence of ICI 182,780, an estrogen receptor (ER) antagonist, CdCl 2 and NaAsO 2 ‐stimulated phosphorylation of ERK1/2 was decreased suggesting that activation is mediated through ERs. To identify the role of the ERs in CdCl 2 and NaAsO 2 ‐induced ERK1/2 phosphorylation, cells were treated with specific inhibitors for ERα, ERβ, and the G‐protein linked estrogen receptor (GPER), and ERK1/2 phosphorylation was measured by immunoblot analysis. The results suggest that CdCl 2 and E 2 activation of MAPK phosphorylation likely involves ERβ whereas ERα may play a minor role in NaAsO 2 ‐stimulated MAPK activation. This study supports the involvement of membrane ER and GPER signaling in mediating cellular responses to environmentally relevant nanomolar concentrations of CdCl 2 and NaAsO 2 in lung adenocarcinoma cells.

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