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Activation of membrane estrogen receptor: MAPK signaling by cadmium chloride and sodium arsenite in human lung adenocarcinoma cells
Ist Teil von
The FASEB journal, 2016-04, Vol.30 (S1)
Erscheinungsjahr
2016
Quelle
Wiley Online Library - AutoHoldings Journals
Beschreibungen/Notizen
Abstract only
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.