Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide maps of H3K4me2 and DNase I hypersensitivity sites in prostate cancer cell line LNCaP and breast cancer cell line MCF-7.

ABSTRACT: We report the high-throughput profiling of histone modification and DNase I hypersensitivity sites in prostate cancer and breaset cancer cells. We found that while AR binding is associated with nucleosome depletion, ER binding is not. We showed that a quantitative measure of DNase I hypersensitivity changes is a powerful tool in indentifying transcription factor cistromes. Examination of histone modification marked nucleosomes and Dnase I hypersensitivity in prostate cancer and breast cancer cells with and without hormone treatment.

ORGANISM(S): Homo sapiens

SUBMITTER: Housheng He 

PROVIDER: E-GEOD-33216 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Differential DNase I hypersensitivity reveals factor-dependent chromatin dynamics.

He Housheng Hansen HH   Meyer Clifford A CA   Chen Mei Wei MW   Jordan V Craig VC   Brown Myles M   Liu X Shirley XS  

Genome research 20120416 6

Transcription factor cistromes are highly cell-type specific. Chromatin accessibility, histone modifications, and nucleosome occupancy have all been found to play a role in defining these binding locations. Here, we show that hormone-induced DNase I hypersensitivity changes (ΔDHS) are highly predictive of androgen receptor (AR) and estrogen receptor 1 (ESR1) binding in prostate cancer and breast cancer cells, respectively. While chromatin structure prior to receptor binding and nucleosome occupa  ...[more]

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