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LM2 cell: infected with lentivirus to stably express Elf5 vs GFP

ABSTRACT: Elf5 induced transcriptional changes in high lung metastasis subline LM2 (MDA-MB-231 origin), control (GFP) vs ELF5

ORGANISM(S): Homo sapiens

PROVIDER: GSE32143 | GEO | 2012/09/20

SECONDARY ACCESSION(S): PRJNA154951

REPOSITORIES: GEO

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LM2 cell: infected with lentivirus to stably express Elf5 vs GFP

Project description:Elf5 induced transcriptional changes in high lung metastasis subline LM2 (MDA-MB-231 origin), control (GFP) vs ELF5 Two-condition experiment, control (GFP) vs Elf5. Each has duplicate biological repeats.

2012-09-20 | E-GEOD-32143 | biostudies-arrayexpress

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MDA-MB-231 cell: infected with lentivirus to stably express mut-Elf5 vs WT-Elf5

Project description:Elf5 induced transcriptional changes in MDA-MB-231 origin, control (mut Elf5) vs WT ELF5

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MDA-MB-231 cell: infected with lentivirus to stably express mut-Elf5 vs WT-Elf5

Project description:Elf5 induced transcriptional changes in MDA-MB-231 origin, control (mut Elf5) vs WT ELF5 Two-condition experiment, control (mut-Elf5) vs WT-Elf5. Each has 3 biological repeats.

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Elf5 inhibits epithelial mesenchymal transition in development and cancer metastasis through transcriptional repression of Snail2

Project description:Elf5 (or ESE-2) is an ETS transcription factor that is abundantly expressed in the mammary epithelium, where it plays a critical role in dictating cell fate and lineage choices. These changes are in part mediated by alterations in the expression and activity of critical components of the Jak/Stat pathway. While the biological function of Elf5 in mammary gland development has been well characterized, its role in breast cancer remains to be elucidated. Here we show that loss of Elf5 leads to features associated with epithelial-mesenchymal transition (EMT) in the mouse mammary gland during pregnancy and lactation. These cellular changes in Elf5-null mammary epithelia are also reflected at the molecular level by the global enrichment of EMT-related gene signatures. ELF5 is expressed in higher level in weakly metastatic breast cancer cells that retained epithelial features compared to highly metastatic cells with mesenchymal features. ELF5 knockdown in T47D breast cancer cells resulted in EMT and increased migration. Conversely, ectopic expression of Elf5 revert mesenchymal-like MDA-MB-231 cells and its lung-tropic variant LM2 to an epithelial phenotype, with reduced migration, invasion and lung metastatic abilities. Finally, we showed that Elf5 binds directly to the promoter of the EMT transcriptional factor Snail2 (Slug) and repress its expression. Taken together, these data established a novel function for Elf5 in inhibiting EMT in normal mammary epithelium and in breast cancer through direct targeting of Snail2. This SuperSeries is composed of the following subset Series: GSE32143: LM2 cell: infected with lentivirus to stably express Elf5 vs GFP GSE32144: MDA-MB-231 cell: infected with lentivirus to stably express mut-Elf5 vs WT-Elf5

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Human breast cancer LM2 cell lines: control vs. MTDH knockdown

Project description:Transcriptional profiling of human breast cancer cell line LM2, a subline of MDA-MB-231 highly metastatic to lung when injected to nude mice, to identify the genes that are regulated after the metastasis gene metadherin is knocked down. Keywords: Genetic modification Empty pSuper vector control cells were compared to the cells transfected with the MTDH knockdown shRNA construct. Two cultured conditions were studied: the LM2 cancer cells were cultured alone or on top of a monolayer of human lung endothelial HMVEC-L cells. Three arrays for each sample.

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RNA sequence analysis to compare Elf5+ and Elf5- tumor cells in C3-T; Elf5-GFP reporter mice tumors

Project description:The data generated here shows increased interferon gamma gene signatures in Elf5- tumor cells in C3-T; Elf5-GFP reporter mice tumors

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Elf5 inhibits epithelial mesenchymal transition in development and cancer metastasis through transcriptional repression of Snail2

2012-09-20 | GSE32150 | GEO