Title : Estrogen receptor α is the major driving factor for growth in tamoxifen-resistant breast cancer and supported by HER/ERK signaling.

Pub. Date : 2013 May

PMID : 23609470






4 Functional Relationships(s)
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1 The EGFR inhibitor gefitinib and the ERK pathway inhibitor U0126 resulted in partial and preferential growth inhibition of tamoxifen-resistant cells. Tamoxifen mitogen-activated protein kinase 1 Homo sapiens
2 The tamoxifen-resistant cells displayed high phosphorylation of ERalpha at Ser118 in the presence of tamoxifen; however, treatment with U0126 neither affected the level of Ser118 phosphorylation nor expression of the ERalpha target Bcl-2, suggesting that ERK contributes to cell growth independently of ERalpha in our cell model. Tamoxifen mitogen-activated protein kinase 1 Homo sapiens
3 Together, these findings demonstrate that ERalpha is a major driver of growth in tamoxifen-resistant cells supported by HER/ERK growth signaling, implying that combined targeting of these pathways may have a clinical potential for overcoming tamoxifen resistance. Tamoxifen mitogen-activated protein kinase 1 Homo sapiens
4 Together, these findings demonstrate that ERalpha is a major driver of growth in tamoxifen-resistant cells supported by HER/ERK growth signaling, implying that combined targeting of these pathways may have a clinical potential for overcoming tamoxifen resistance. Tamoxifen mitogen-activated protein kinase 1 Homo sapiens