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RNA-seq data of T47D overexpressing prolactin and the control

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

PROVIDER: PRJNA914234 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22827112.fastq.gz	Fastqsanger.gz
	SRR22827113.fastq.gz	Fastqsanger.gz
	SRR22827114.fastq.gz	Fastqsanger.gz
	SRR22827115.fastq.gz	Fastqsanger.gz
	SRR22827116.fastq.gz	Fastqsanger.gz

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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.

2023-03-01 | GSE221394 | GEO

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.

2020-06-03 | GSE151635 | GEO

miRNA Expression data from WASF3 overexpressing stable T47D cells and control cells

Project description:We recently showed that inactivation of the WASF3/WAVE3 gene in breast cancer cells results in loss of cell motility and invasion in vitro and metastasis in vivo. To obtain a better understanding of molecular mechanisms of action of WASF3, we have established the stable WASF3 overexpressing T47D cells using lentiviral infect system. We used miRNA microarrays to detail the global programme of miRNA expression after overexpression of WASF3 and identified distinct classes of up or down-regulated metastmir associated with breast cancer cell migration and motility invasion

2014-08-19 | GSE31367 | GEO

Expression data from T47D/S2 (control) and T47D/TR-2 (tamoxifen-resistant) cell lines

Project description:Expression data from T47D/S2 (control) and T47D/TR-2 (tamoxifen-resistant) cell lines

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

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

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Effect of diptoindonesin G on T47D cells overexpressing the Y537S ER mutation

Project description:To investigate the effect of diptoindonesin G on breast cancer cells expressing the estrogen receptor Y537S ligand binding domain mutation, we treated T47D cells overexpressing the ER Y537S mutation and treated them with vehicle or diptoindonesin G and performed differential gene expression analysis and gene set enrichment analysis

2022-06-11 | GSE205716 | GEO

Transriptome profiling of breast cancer cells T47D overexpressing ZNF528-AS1

Project description:Transriptome profiling of breast cancer cells T47D overexpressing ZNF528-AS1

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Expression data from Min6 cells overexpressing control or SPARC adenovirus

Project description:Expression data from Min6 cells overexpressing control or SPARC adenovirus

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Expression data with either EglN2 or control knockdown in T47D cells

Project description:In order to perform integrated analysis for EglN2 ChIP-Seq and microarray to identify EglN2 direct target genes, we performed the microarray analysis for T47D breast cancer cells with either control or EglN2 siRNA followed by hypoxia+DMOG treatment

2014-07-31 | GSE59936 | GEO

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.

2010-06-17 | GSE22363 | GEO

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