Details

Autor(en) / Beteiligte

• Hyzer, Jeffrey M.
• Krauss, Katazyna A.
• Black, Austin T.
• Todd, Sarah L.
• Elpers, Julia T.
• Hoerter, Jacob E.
• Klinge, Carolyn M.
• Huff, Mary O.

Titel

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.