Abstract
The adaptor protein NHERF1/EBP50 (Na/H exchanger regulatory factor 1/ezrin-radixin-moesin-binding phosphoprotein 50) emerged recently as an important player in breast cancer progression. Consisting of two tandem PDZ domains linked to a carboxyl-terminal ezrin-binding region, NHERF1 assembles macromolecular complexes at the apical membrane of epithelial cells in many epithelial tissues, including the mammary gland. Involved initially in trafficking and regulation of transmembrane ion transporters and G protein-coupled receptors, NHERF1 also couples molecules involved in cell growth, such as the platelet-derived growth factor receptor (PDGFR) and PTEN (phosphatase and tensin homolog deleted on chromosome 10). In the previous issue of Breast Cancer Research, Pan and colleagues show an inhibitory action of NHERF1 on the phosphoinositide-3 kinase (PI3K)/Akt pathway in breast cancer cells via interaction of NHERF1 with PTEN, the physiological antagonist of the PI3K. Additionally, they show that NHERF1 expression confers susceptibility to PDGFR pharmacological inhibition depending on the presence of PTEN tumor suppressor.
Highlights
Breast cancer is a complex disease comprising multiple pathological types and molecular profiles that determine various clinical outcomes and responses to therapy
New oncogenic pathways are studied for their potential to become therapeutic molecular targets, one such pathway being the phosphoinositide-3 kinase (PI3K)/Akt pathway that is physiologically repressed by the PTEN tumor suppressor in normal tissues and cells
In the previous issue of Breast Cancer Research, Pan and colleagues [1] show that Na/H exchanger regulatory factor 1 (NHERF1), an adaptor protein recently shown to be involved in the progression of breast cancer, acts as a brake on the PI3K signaling downstream of the platelet-derived growth factor receptor (PDGFR) in the mammary gland
Summary
Breast cancer is a complex disease comprising multiple pathological types and molecular profiles that determine various clinical outcomes and responses to therapy. In the previous issue of Breast Cancer Research, Pan and colleagues show an inhibitory action of NHERF1 on the phosphoinositide-3 kinase (PI3K)/Akt pathway in breast cancer cells via interaction of NHERF1 with PTEN, the physiological antagonist of the PI3K.
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