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Gene expression by high-throughput sequencing of T47D-MTVL human breast cancer cells upon H1.4 knock-down and multiple H1 variants

ABSTRACT: Gene expression of T47D-MTVL human breast cancer cells expressing Dox-inducible shRNAs against histone H1.4 (120sh) or multiple H1 variants (225sh)

ORGANISM(S): Homo sapiens

PROVIDER: GSE83277 | GEO | 2017/08/14

SECONDARY ACCESSION(S): PRJNA325483

REPOSITORIES: GEO

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Gene expression of T47D-MTVL human breast cancer cells upon H1.4 knock-down or overexpression

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Gene expression of T47D-MTVL human breast cancer cells upon H1.4 knock-down or overexpression

Project description:Gene expression of T47D-MTVL human breast cancer cells expressing Dox-inducible shRNAs against histone H1.4 (sh120) or multiple H1 variants (sh225), or overexpressing WT or K26A mutant HA-tagged H1.4. T47D-MTVL, breast cancer cell line carrying one stably integrated copy of luciferase reporter gene driven by the MMTV promoter, is stably infected with an inducible system for the expression of shRNAs.Cells stably express RedFP and KRAB repressor fused to Tet regulator.Upon Dox treatment, cells express RedFP and the cloned shRNA. Stable breast cancer-derived cell lines expressing an shRNA against one of each of the histone H1 isoforms in response to doxycycline (Dox) were grown for six days in the presence or absence of Dox, in duplicate, and RNA extracted for microarray hybridization. Cell lines used: inducible shRNA against H1.4 or multiple H1 variants, and random shRNA-expression vector. Stable breast cancer-derived cell lines expressing the histone H1.4 isoform, WT or K26A, HA-tagged, in duplicate, and RNA extracted for microarray hybridization. Cell lines used: overexpressing H1.4 WT or K26A mutant.

2014-05-16 | E-GEOD-55786 | biostudies-arrayexpress

Chromatin-enriched RNAs expression profiling by high-throughput sequencing of T47D-MTVL human breast cancer cells

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Genome-wide profiling of histone H1 variants and H3K9me3 in T47D-MTVL cells upon multiple H1 depletion

Project description:Human somatic cells may contain up to seven members of the histone H1 family contributing to chromatin compaction and regulation of nuclear processes, apparently with certain subtype specificities. In breast cancer cells, the combined depletion of H1.2 and H1.4 has a strong deleterious effect, deregulates many genes, promotes the appearance of accessibility sites genome-wide, and triggers an interferon response via activation of heterochromatic repeats. We have further analyzed the consequences of multiple H1 variants depletion by profiling the occupancy of five somatic histone H1 variants and H3K9me3 post-translational modification in T47D-MTVL cancer cells. Specifically, stable breast cancer-derived cell lines expressing an shRNA against multiple histone H1 isoforms in response to doxycycline (Dox) were grown for six days in the presence or absence of Dox. ChIP-Seq experiments were subsequently performed to analyze the genome-wide localization of histone H1 variants and H3K9me3.

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Gene expression of T47D-MTVL human breast cancer cells upon H1X knock-down

Project description:Gene expression of T47D-MTVL human breast cancer cells expressing Dox-inducible shRNAs against histone H1X

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Analysis of the DNA topology upon multiple histone H1 variants depletion by Hi-C experiments

Project description:The combined depletion of histones H1.2 and H1.4 in T47D-MTVL human breast cancer cells has a strong deleterious effect, deregulates gene expression, promotes the appearance of genome-wide accessibility sites, and triggers the interferon response. We have further analyzed the consequences of multiple H1 variants depletion at the topological level by performing Hi-C experiments on T47D-MTVL cancer cells expressing a Dox-inducible shRNA against multiple H1 variants.

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Gene expression profiling by high-throughput sequencing of T47D-MTVL human breast cancer cells upon H1X knock-down

Project description:Gene expression of T47D-MTVL human breast cancer cells expressing Dox-inducible shRNAs against histone H1X (H1Xsh).

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Analysis of the DNA topology in T47D-MTVL cells by Hi-C data

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