Breast cancer (BC) is linked to estrogen exposure. Estradiol (E2) stimulates BC cells proliferation by binding the estrogen receptor (ER). Hormone-related cancers have been linked to estrogenic environmental contaminants. Cadmium (Cd) a toxic pollutant, acts as estrogens in BC cells. Purpose of our study was to evaluate whether Cd regulates MCF-7 cell proliferation by activating ERK1/2, Akt and PDGFRalpha kinases. Cd increased cell proliferation and the ER-antagonist ICI 182,780 blunted it. To characterize an ER-dependent mechanism, ERalpha/beta expression was evaluated. Cd decreased ERalpha expression, but not ERbeta. Cd also increased ERK1/2, Akt and PDGFRalpha phosphorylation while ICI blocked it. Since stimulation of phosphorylation was slower than expected, c-fos and c-jun proto-oncogenes, and PDGFA were analyzed. Cd rapidly increased c-jun, c-fos and PDGFA expression. Cells were also co-incubated with the Cd and specific kinases inhibitors, which blocked the Cd-stimulated proliferation. In conclusion, our results indicate that Cd increases BC cell proliferation in vitro by stimulating Akt, ERK1/2 and PDGFRalpha kinases activity likely by activating c-fos, c-jun and PDGFA by an ERalpha-dependent mechanism.

Cadmium induces mitogenic signaling in breast cancer cell by an ERalpha-dependent mechanism / Brama, M; Gnessi, Lucio; Basciani, Sabrina; Cerulli, N; Politi, Laura; G., Spera; Mariani, S; Cherubini, S; SCOTTO D'ABUSCO, Anna; Scandurra, R; Migliaccio, S.. - In: MOLECULAR AND CELLULAR ENDOCRINOLOGY. - ISSN 0303-7207. - 264:(2007), pp. 102-108. [10.1016/j.mce.2006.10.013]

Cadmium induces mitogenic signaling in breast cancer cell by an ERalpha-dependent mechanism.

GNESSI, Lucio;BASCIANI, Sabrina;POLITI, Laura;MARIANI S;SCOTTO D'ABUSCO, ANNA;MIGLIACCIO S.
2007

Abstract

Breast cancer (BC) is linked to estrogen exposure. Estradiol (E2) stimulates BC cells proliferation by binding the estrogen receptor (ER). Hormone-related cancers have been linked to estrogenic environmental contaminants. Cadmium (Cd) a toxic pollutant, acts as estrogens in BC cells. Purpose of our study was to evaluate whether Cd regulates MCF-7 cell proliferation by activating ERK1/2, Akt and PDGFRalpha kinases. Cd increased cell proliferation and the ER-antagonist ICI 182,780 blunted it. To characterize an ER-dependent mechanism, ERalpha/beta expression was evaluated. Cd decreased ERalpha expression, but not ERbeta. Cd also increased ERK1/2, Akt and PDGFRalpha phosphorylation while ICI blocked it. Since stimulation of phosphorylation was slower than expected, c-fos and c-jun proto-oncogenes, and PDGFA were analyzed. Cd rapidly increased c-jun, c-fos and PDGFA expression. Cells were also co-incubated with the Cd and specific kinases inhibitors, which blocked the Cd-stimulated proliferation. In conclusion, our results indicate that Cd increases BC cell proliferation in vitro by stimulating Akt, ERK1/2 and PDGFRalpha kinases activity likely by activating c-fos, c-jun and PDGFA by an ERalpha-dependent mechanism.
2007
01 Pubblicazione su rivista::01a Articolo in rivista
Cadmium induces mitogenic signaling in breast cancer cell by an ERalpha-dependent mechanism / Brama, M; Gnessi, Lucio; Basciani, Sabrina; Cerulli, N; Politi, Laura; G., Spera; Mariani, S; Cherubini, S; SCOTTO D'ABUSCO, Anna; Scandurra, R; Migliaccio, S.. - In: MOLECULAR AND CELLULAR ENDOCRINOLOGY. - ISSN 0303-7207. - 264:(2007), pp. 102-108. [10.1016/j.mce.2006.10.013]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/237053
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