We are analyzing https://link.springer.com/article/10.1007/s10549-005-1483-4.

Title:
GREB1 is a critical regulator of hormone dependent breast cancer growth | Breast Cancer Research and Treatment
Description:
Background Estrogen plays a central role in breast cancer pathogenesis and many potent risk factors for the development of the disease can be explained in terms of increased lifetime exposure to estrogen. Although estrogen regulated genes have been identified, those critically involved in growth regulation remain elusive. Methods. To identify candidate genes involved in estrogen stimulated breast cancer growth, DNA microarray based gene expression profiles were generated from three estrogen receptor α (ERα) positive breast cancer cell lines grown under multiple stimulatory and inhibitory conditions. Results Only three genes were significantly induced by 17β-estradiol (E2) relative to control in all three cell lines: GREB1, stromal cell-derived factor 1 (SDF-1) and trefoil factor 1 (pS2). Quantitative real-time PCR assays confirmed that in all three cell lines, GREB1 was induced by E2, but not by the antiestrogens tamoxifen (TAM) or ICI 182,780. GREB1 expression level was strongly correlated with ERα positivity in 39 breast cancer cell lines of known ERα expression status. GREB1 induction by E2 was rapid (7.3 fold by 2 h for MCF-7) and mirrored the fraction of cells entering S-phase when released from an estrogen deprivation induced cell arrest. Suppression of GREB1 using siRNA blocked estrogen induced growth in MCF-7 cells and caused a paradoxical E2 induced growth inhibition. Conclusion These data suggest that GREB1 is critically involved in the estrogen induced growth of breast cancer cells and has the potential of being a clinical marker for response to endocrine therapy as well as a potential therapeutic target.
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Keywords {🔍}

cancer, breast, google, scholar, estrogen, growth, greb, expression, receptor, cells, article, genes, gene, res, cell, factor, human, induced, access, rae, response, privacy, cookies, content, data, research, lippman, lines, tamoxifen, target, usa, mol, endocrinol, profiling, publish, search, johnson, erα, control, mcf, open, receptors, treat, cdna, nature, analysis, information, log, journal, treatment,

Topics {✒️}

real-time quantitative pcr month download article/chapter transforming growth factor-α breast cancer cells cells entering s-phase early estrogen-induced gene human osteosarcoma cells clark-lewis df legler estradiol-independent mrna control pnr-2/ps2 immunohistochemical staining 4-hydroxy-n-desmethyl tamoxifen growth factor pathways breast cancer pathogenesis breast cancer er ps2 gene transcription estrogen induced growth related subjects estrogen-regulated gene expression dunphy po brown estrogen-regulated genes expressed soulez mg parker unidentified human genes stossi jm danes estrogen receptor α estrogen receptor action estrogen receptor β estrogen-responsive genes breast cancer mcf-7 cells brown jm jeltsch schwartz jm heard potent risk factors estrogen regulated genes privacy choices/manage cookies usa james full article pdf trefoil factor 1 regulated gene expression sci 1 frasor jm danes rowlatt tc stephens bessia jl virelizier common target genes model-based analysis lyttle cr katzenellenbogen bs cell lines gene expression profiling check access instant access

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         headline:GREB1 is a critical regulator of hormone dependent breast cancer growth
         description:Background Estrogen plays a central role in breast cancer pathogenesis and many potent risk factors for the development of the disease can be explained in terms of increased lifetime exposure to estrogen. Although estrogen regulated genes have been identified, those critically involved in growth regulation remain elusive. Methods. To identify candidate genes involved in estrogen stimulated breast cancer growth, DNA microarray based gene expression profiles were generated from three estrogen receptor α (ERα) positive breast cancer cell lines grown under multiple stimulatory and inhibitory conditions. Results Only three genes were significantly induced by 17β-estradiol (E2) relative to control in all three cell lines: GREB1, stromal cell-derived factor 1 (SDF-1) and trefoil factor 1 (pS2). Quantitative real-time PCR assays confirmed that in all three cell lines, GREB1 was induced by E2, but not by the antiestrogens tamoxifen (TAM) or ICI 182,780. GREB1 expression level was strongly correlated with ERα positivity in 39 breast cancer cell lines of known ERα expression status. GREB1 induction by E2 was rapid (7.3 fold by 2 h for MCF-7) and mirrored the fraction of cells entering S-phase when released from an estrogen deprivation induced cell arrest. Suppression of GREB1 using siRNA blocked estrogen induced growth in MCF-7 cells and caused a paradoxical E2 induced growth inhibition. Conclusion These data suggest that GREB1 is critically involved in the estrogen induced growth of breast cancer cells and has the potential of being a clinical marker for response to endocrine therapy as well as a potential therapeutic target.
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      description:Background Estrogen plays a central role in breast cancer pathogenesis and many potent risk factors for the development of the disease can be explained in terms of increased lifetime exposure to estrogen. Although estrogen regulated genes have been identified, those critically involved in growth regulation remain elusive. Methods. To identify candidate genes involved in estrogen stimulated breast cancer growth, DNA microarray based gene expression profiles were generated from three estrogen receptor α (ERα) positive breast cancer cell lines grown under multiple stimulatory and inhibitory conditions. Results Only three genes were significantly induced by 17β-estradiol (E2) relative to control in all three cell lines: GREB1, stromal cell-derived factor 1 (SDF-1) and trefoil factor 1 (pS2). Quantitative real-time PCR assays confirmed that in all three cell lines, GREB1 was induced by E2, but not by the antiestrogens tamoxifen (TAM) or ICI 182,780. GREB1 expression level was strongly correlated with ERα positivity in 39 breast cancer cell lines of known ERα expression status. GREB1 induction by E2 was rapid (7.3 fold by 2 h for MCF-7) and mirrored the fraction of cells entering S-phase when released from an estrogen deprivation induced cell arrest. Suppression of GREB1 using siRNA blocked estrogen induced growth in MCF-7 cells and caused a paradoxical E2 induced growth inhibition. Conclusion These data suggest that GREB1 is critically involved in the estrogen induced growth of breast cancer cells and has the potential of being a clinical marker for response to endocrine therapy as well as a potential therapeutic target.
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