Abstract
[This corrects the article DOI: 10.18632/oncotarget.1795.].
Highlights
70% of breast tumors express estrogen receptor alpha (ERalpha) [1, 2]
To study the regulation of MitogenActivated Protein Kinase Phosphatases (MKPs) and their effect on Mitogen-Activated Protein Kinases (MAPKs) signaling in tamoxifen sensitivity, we identified a cell line model suitable for expression of exogenous MKP proteins
We show here that treatment with TAM stimulates the expression of MKP-2, but does not have the same effect on MKP-1
Summary
70% of breast tumors express estrogen receptor alpha (ERalpha) [1, 2]. For women who present with ERalpha-positive tumors, first-line therapy involves treatment with tamoxifen. 30-50% of women with metastatic disease will experience temporary remission while being treated with tamoxifen [3, 4] Most of these women will eventually develop recurrent disease that is resistant to tamoxifen treatment. There are many proposed mechanisms of tamoxifen resistance, including, but not limited to, ligand-independent activation of the estrogen receptor [1] and tamoxifen acting as an agonist via crosstalk with other transcription factors [5]. Both of these resistance mechanisms have been connected to the activity of extracellular signal regulated kinases (ERK), one of the Mitogen-Activated Protein Kinases (MAPKs) [1, 5]. Pharmacological inhibition of ERK activity in vitro has been shown to reverse the tamoxifen resistant phenotype in breast [10] and several other cancer types [11, 12]
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