Estrogen receptor β role in tumour suppression of triple negative breast cancer
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB33041 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3375350.fastq.gz | Fastqsanger.gz | |||
| ERR3375360.fastq.gz | Fastqsanger.gz | |||
| ERR3375351.fastq.gz | Fastqsanger.gz | |||
| ERR3375361.fastq.gz | Fastqsanger.gz | |||
| ERR3375352.fastq.gz | Fastqsanger.gz |
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Project description:Estrogen receptor β role in tumour suppression of triple negative breast cancer - ChIPseq experiment
| PRJEB33056 | ENA
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
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.
2019-12-02 | E-MTAB-8056 | biostudies-arrayexpress
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.
2019-12-03 | PXD014468 | Pride
Project description:The goal of this work was to identify all estrogen receptor beta target genes using RNA sequencing in MDA-MB-468 triple negative breast cancer cells engineered with inducible expression of full length estrogen receptor beta.
2015-08-12 | GSE71960 | GEO
Project description:The standard of care for triple-negative breast cancer is chemotherapy followed by surgical resection, and in most cases, additional rounds of chemotherapy treatment. While highly effective, approximately half of patients will experience disease recurrence that does not respond to additional rounds of treatment. Previous findings demonstrate that estrogen receptor beta (ERb) is expressed in upwards of 20% of triple-negative tumors, and that ERb functions as a tumor suppressor in triple-negative breast cancer models, it was of interest to determine if the tumor-suppressive effects of ERb persisted in chemo-therapy-resistant forms of the disease. Here, we demonstrate that the activation of ERb in chemotherapy-resistant triple-negative breast cancer cell lines elicits equivalent or superior inhibitory effects compared to chemotherapy-sensitive counterparts. These findings support the potential use of ERb-targeting agents in advanced forms of the disease.
2025-07-01 | GSE300447 | GEO
Project description:Targeted therapies for triple-negative breast cancer have increased the number of available treatment options for patients. However, an optimal treatment strategy is still an unmet medical need due to the lack of targetable biomarkers and tumour heterogeneity. Aptamers have high selectivity and specificity towards target proteins. Lower molecular weight, increased stability, less immunogenicity, and rapid tissue uptake make aptamers an attractive alternative to antibodies. Attempts to develop aptamer therapeutics have shown difficulties translating in vitro results to in vivo. Aptamer GreenB1 exhibits selectivity to triple-negative MDA-MB-231 human breast cancer cell line in vitro compared to estrogen, progesterone, and glucocorticoid receptor-expressing MCF-7 human breast cancer cell line. The aptamer is rapidly internalised into cells and trafficked to lysosomes. Here, we identify 1-integrin as the target protein for GreenB1 using proximity labelling and mass spectrometry proteomics. GreenB1 homes preferentially to the tumour in the 4T1 triple-negative breast cancer mice model in vivo.
2023-08-24 | PXD034982 | Pride
Project description:The goal of this work was to identify all estrogen receptor beta target genes using RNA sequencing in MDA-MB-468 triple negative breast cancer cells engineered with inducible expression of full length estrogen receptor beta. MDA-MB-468 breast cancer cells with inducible ERb expression (MDA-468-ERb cells) were treated in triplicate with vehicle (control, no ERb) or doxycycline (plus ERb) for 48 hr prior to treatment with 0.1% DMSO vehicle or 10 nM 17b-estradiol for 4 hr.
2015-08-12 | E-GEOD-71960 | biostudies-arrayexpress
Project description:Purpose: To characterize the expression of phosphatases in estrogen receptor negative breast cancer Little is known about the role of phosphatases in the major estrogen receptor negative breast cancer phenotypes (i.e. those overexpressing ERBB2 and the triple negative). We carried out microarray phosphatome profiling in 41 estrogen receptor negative (ER-) breast cancer patients (as determined by immunohistochemistry (IHC)) containing both ERBB2+ and ERBB2- in order to characterize the differences between these groups by Statistical Analysis of Microarrays (SAM). Our findings point to the importance of the MAPK and PI3K pathways in ER- BCs as some of the most differentially expressed phosphatases (like DUSP4 and DUSP6) share ERK as substrate, or regulate the PI3K pathway (INPP4B, PTEN). These observations are also confirmed by pathway and GSEA analysis. It is shown that both ER- ERBB2+ and triple negative breast cancers have a distinctive pattern of phosphatase RNA expression. Surgical specimens from primary breast cancers that were estrogen receptor negative according to immunohistochemistry
2014-06-30 | E-GEOD-51999 | biostudies-arrayexpress
Project description:We performed whole transcriptome sequencing of human monocytes that were co-cultured with estrogen receptor positive (ER+) or triple-negative (TNBC) breast cancer cell lines and studied the biological responses related to the differential gene activation in both cell types to understand how different cancer cells educate host cells to support tumor growth
2015-11-19 | GSE75130 | GEO