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See Latest ArticlesMenin, a product of the MENI gene, binds to estrogen receptor to enhance its activity in breast cancer cells: possibility of a novel predictive factor for tamoxifen resistance
Breast Cancer Research and Treatment, 11/04/09
Imachi H et al. – Menin can function as a transcriptional regulator of ER? and is a possible predictive factor for tamoxifen resistance.
Methods- Menin is a tumor suppressor encoded by Men1 that is mutated in the human-inherited tumor syndrome multiple endocrine neoplasia type 1 (MEN1); it also serves as a critical link in the recruitment of nuclear receptor-mediated transcription.
- Menin expressed in breast cancer cell line MCF-7 is colocalized with ER? and functions as a direct coactivator of ER-mediated transcription in breast cancer cells
- In MCF-7 cells, coexpression of menin and estrogen-response element-luciferase induced the activity of the latter in a hormone-dependent manner
- Cells knocked down for ER? exhibited impaired ERE-luciferase activity induced by menin
- Mammalian two-hybrid assay and GST pull-down assays indicated that menin could interact with the AF-2 domain of ER?
- Tamoxifen inhibited the binding of menin to AF-2 in mammalian two-hybrid assay, but in menin-overexpressing clones, tamoxifen suppressed ERE-luciferase activity only to the levels of nontreated wild-type MCF-7
- In a clinical study with 65 ER-positive breast cancer samples—all of which had been treated with tamoxifen for 2–5 years as adjuvant therapies—menin-positive tumors had a worse outcome than menin-negative ones
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Today in Breast...keeping you current
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