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Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB signaling in triple negative breast cancer

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE155686 | GEO | 2020/09/30

REPOSITORIES: GEO

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Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB signaling in triple negative breast cancer [RNA-Seq]

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Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB signaling in triple negative breast cancer [ChIP-Seq]

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Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB signaling in triple negative breast cancer

Project description:Estrogen receptor beta repurposes EZH2 to suppress oncogenic NFκB signaling in triple negative breast cancer

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Estrogen Receptor beta (ERβ) interactome in triple negative breast cancer cells nuclei

Project description:Breast cancer (BC) is the second most common type of cancer in women and one of the leading causes of cancer-related deaths worldwide. BC classification is based on the detection of three main histological markers: estrogen receptor alpha (ERα), progesterone receptor (PR) and the amplification of epidermal growth factor receptor 2 (HER2/neu). A specific BC subtype, named triple-negative BC (TNBC), lacks the aforementioned markers but a fraction of them express the estrogen receptor beta (ERβ). To investigate the functional role of ERβ in these tumors, interaction proteomics coupled to mass spectrometry (MS) was applied to deeply characterize the nuclear interactors partners in MDA-MD-468 and HCC1806 TNBC cells.

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Estrogen receptor β role in tumour suppression of triple negative breast cancer

Project description:Breast cancer (BC) is the most common cancer in women worldwide, and is classified in multiple subtypes, including the so called triple-negative BC (TNBC). This is characterized by lack of estrogen receptor alpha (ERα), progesterone receptor (PR) and epidermal growth factor receptor 2 (HER2/neu), that represent common targets for BC treatment. Their absence limits the number of therapies that may be applied for TNBC treatment, suggesting the need to identify novel therapeutic targets against this disease. Several studies reported that the beta ER subtype (ERβ) is expressed in a sizeable fraction of TNBCs where its presence correlates with improved patient outcome. We evaluated ERβ expression in TNBC tissues by immunohistochemistry using two validated antibodies, demonstrating presence of this protein in 28% of samples. To investigate, in this context, the role of this estrogen receptor in TNBC biology, ERβ-expressing cell lines, representing different TNBC subtypes, were generated. Cellular and functional assays confirmed the antiproliferative activity of ERβ in TNBCs. Interaction proteomics revealed in BC nuclei the presence of several protein complexes associated with this receptor involved in chromatin remodeling, miRNA maturation and mRNA transcription. Transcriptome analyses pointed out tumor subtype-specific signaling pathways deregulation. Interestingly, among these the cholesterol biosynthesis pathway was commonly downregulated in all cell lines tested. Global analyses of ERβ binding to the genome showed its recruitment to regulatory sites of Sterol Regulatory Element-Binding Protein 1 (SREBP1), indicating a direct regulation of this pathway by the receptor. These findings suggest that drugs targeting components of cholesterol biosynthesis pathway may be new potential therapeutic options for TNBC treatment.

2019-12-03 | E-MTAB-8055 | biostudies-arrayexpress

Estrogen receptor β role in tumour suppression of triple negative breast cancer - ChIPseq experiment

2019-12-02 | E-MTAB-8056 | biostudies-arrayexpress

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