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• W4362490885 abstract "<div>Abstract<p>Brain metastasis from breast cancer is an increasingly important clinical problem. Here we assessed the role of CD44^hi/CD24^lo cells and pathways that regulate them, in an experimental model of brain metastasis. Notch signaling (mediated by γ-secretase) has been shown to contribute to maintenance of the cancer stem cell (CSC) phenotype. Cells sorted for a reduced stem-like phenotype had a reduced ability to form brain metastases compared with unsorted or CD44^hi/CD24^lo cells (<i>P</i> < 0.05; Kruskal–Wallis). To assess the effect of γ-secretase inhibition, cells were cultured with DAPT and the CD44/CD24 phenotypes quantified. 231-BR cells with a CD44^hi/CD24^lo phenotype was reduced by about 15% in cells treated with DAPT compared with DMSO-treated or untreated cells (<i>P</i> = 0.001, ANOVA). <i>In vivo</i>, mice treated with DAPT developed significantly fewer micro- and macrometastases compared with vehicle treated or untreated mice (<i>P</i> = 0.011, Kruskal–Wallis). Notch1 knockdown reduced the expression of CD44^hi/CD24^lo phenotype by about 20%. <i>In vitro</i>, Notch1 shRNA resulted in a reduction in cellular growth at 24, 48, and 72 hours time points (<i>P</i> = 0.033, <i>P</i> = 0.002, and <i>P</i> = 0.009, ANOVA) and about 60% reduction in Matrigel invasion was observed (<i>P</i> < 0.001, ANOVA). Cells transfected with shNotch1 formed significantly fewer macrometastases and micrometastases compared with scrambled shRNA or untransfected cells (<i>P</i> < 0.001; Kruskal–Wallis). These data suggest that the CSC phenotype contributes to the development of brain metastases from breast cancer, and this may arise in part from increased Notch activity. <i>Mol Cancer Res; 9(7); 834–44. ©2011 AACR</i>.</p></div>" @default.
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• W4362490885 date "2023-04-03" @default.
• W4362490885 modified "2023-10-06" @default.
• W4362490885 title "Data from Notch1 Inhibition Alters the CD44^hi/CD24^lo Population and Reduces the Formation of Brain Metastases from Breast Cancer" @default.
• W4362490885 doi "https://doi.org/10.1158/1541-7786.c.6542164.v1" @default.
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