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Gene expression data from T47D human breast ductal carcinoma cells treated with prolactin and/or NIM811

ABSTRACT: Gene expression data from T47D human breast ductal carcinoma cells treated with prolactin and/or NIM811

PROVIDER: PRJNA636697 | ENA |

REPOSITORIES: ENA

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Gene expression data from T47D human breast ductal carcinoma cells treated with prolactin and/or NIM811

Project description:The hormone prolactin is implicated in the pathogenesis of breast cancer, and a subset of prolactin-induced gene expression is mediated by CypA activity. The non-immunosuppressive prolyl isomerase inhibitor, NIM811, is an inhibitor of CypA. We used NIM811 in combination with prolactin treatment in T47D cells to determine differential expression under these conditions.

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RNA-seq data of T47D overexpressing prolactin and the control

Project description:The exact role of prolactin on breast cancer still remains unclear. Clues supportive or unsurpportive for prolactin to be cancer driver are confusing. To clarify the role of autocrine prolactin of breast cancer cells on cancer development, we construct T47D cells overexpressing prolactin.

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RNA-seq data of T47D overexpressing prolactin and the control

Project description:RNA-seq data of T47D overexpressing prolactin and the control

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Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer

Project description:This SuperSeries is composed of the following subset Series: GSE41194: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 1) GSE41196: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 2) GSE41197: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 3) GSE41198: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 4 stroma) GSE41227: Differentially Expressed Genes Regulating the Progression of Ductal Carcinoma In Situ to Invasive Breast Cancer (Group 4 Epithelial) Refer to individual Series

2012-09-29 | E-GEOD-41228 | biostudies-arrayexpress

Effects of estradiol, progesterone, prolactin and oxytocin on miRNA levels in T47D human breast cells

Project description:Effects of estradiol, progesterone, prolactin and oxytocin on miRNA levels in T47D human breast cells

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Effects of estradiol, progesterone, prolactin and oxytocin on miRNA levels in T47D human breast cells

Project description:The aim of the project was to analyse the levels of miRNA upon hormonal treatment in T47D breast cells

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Gene expression data from MCF7 breast adenocarcinoma cells treated with prolactin and/or bufexamac

Project description:The hormone prolactin is implicated in the pathogenesis of breast cancer, and a subset of prolactin-induced gene expression is mediated by HDAC6 activity. The NSAID, bufexamac, is a fairly specific inhibitor of HDAC6 and HDAC10. We used bufexamac in combination with prolactin treatment in MCF7 cells to determine differential expression under these conditions.

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Expression data for EglN2 conditional knockdown in T47D breast carcinoma cells

Project description:mRNA expression was assayed from T47D SCR and T47D EGLN2 conditional knock down cell lines in order to profile the gene expression pattern regulated by EGLN2.

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The anti-proliferative effects of progestins in T47D breast cancer cells are tempered by progestin-induction of the ETS transcription factor Elf5.

Project description:Prolactin and progesterone act together to regulate mammary alveolar development, and both hormones have been implicated in breast cancer initiation and progression. Here we show that Elf5, a prolactin-induced ETS transcription factor that specifies the mammary secretory cell lineage, is also induced by progestins in breast cancer cells via a direct mechanism. To define the transcriptional response to progestin elicited via Elf5 we made an inducible Elf5 sh-RNA knock down model in T47D breast cancer cells and used it to prevent the progestin-induction of Elf5. Functional analysis of Affymetrix gene expression data using Gene Ontologies and Gene Set Enrichment Analysis showed enhancement of the progestin effects on cell cycle gene expression. Cell proliferation assays showed a more efficacious progestin-induced growth arrest when Elf5 was kept at baseline levels. These results showed that progestin-induction of Elf5 expression tempered the anti-proliferative effects of progestins in T47D cells, providing a further mechanistic link between prolactin and progestin in the regulation of mammary cell phenotype.

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The anti-proliferative effects of progestins in T47D breast cancer cells are tempered by progestin-induction of the ETS transcription factor Elf5.

2010-07-08 | E-GEOD-22363 | biostudies-arrayexpress