Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Proteasome inhibition blocks estrogen-dependent gene transcription by decreasing histone H2B monoubiquitination in human breast cancer cells

ABSTRACT: The estrogen receptor-alpha (ERα) determines breast cancer cell phenotype and is a prognostic indicator. A better understanding of the mechanisms controlling ERα function may uncover improved strategies for the treatment of breast cancer. Proteasome inhibition was previously reported to regulate estrogen-induced transcription but the mechanisms by which it influences ERα function remain controversial. In this study we investigated the transcriptome-wide effects of the proteasome inhibitor Velcade on estrogen-regulated transcription in MCF7 human breast cancer cells and demonstrate a specific global decrease in estrogen-induced transcription. This set contains 12 microarray samples. 3 controls, 3 estrogen stimulated, 3 Bortezomib stimulated, 3 Bortezomib + estrogen stimulated

ORGANISM(S): Homo sapiens

SUBMITTER: Frank Kramer 

PROVIDER: E-GEOD-30931 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Estrogen-dependent gene transcription in human breast cancer cells relies upon proteasome-dependent monoubiquitination of histone H2B.

Prenzel Tanja T   Begus-Nahrmann Yvonne Y   Kramer Frank F   Hennion Magali M   Hsu Chieh C   Gorsler Theresa T   Hintermair Corinna C   Eick Dirk D   Kremmer Elisabeth E   Simons Mikael M   Beissbarth Tim T   Johnsen Steven A SA  

Cancer research 20110823 17

The estrogen receptor-α (ERα) determines the phenotype of breast cancers where it serves as a positive prognostic indicator. ERα is a well-established target for breast cancer therapy, but strategies to target its function remain of interest to address therapeutic resistance and further improve treatment. Recent findings indicate that proteasome inhibition can regulate estrogen-induced transcription, but how ERα function might be regulated was uncertain. In this study, we investigated the transc  ...[more]

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