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Transposase-accessible chromatin regions of MDA-MB-453 cells expressing ectopic wild-type, Y537S, or K303R ER alpha.

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE191065 | GEO | 2022/12/16

REPOSITORIES: GEO

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Genome-wide analysis of transposase-accessible chromatin regions of MDA-MB-453 cells expressing ectopic wild-type, Y537S, or K303R ER alpha.

Project description:We analyzed the chromatin state of MDA-MB-453 cells expressing wild-type, Y537S, or K303R ER alpha by ATAC-seq, and identified K303R-related disordered chromatin opening which has Fox-binding motifs.

2022-12-16 | GSE191057 | GEO

Transposase-accessible chromatin regions of MDA-MB-453 cells expressing ectopic wild-type, Y537S, or K303R ER alpha.

Project description:Transposase-accessible chromatin regions of MDA-MB-453 cells expressing ectopic wild-type, Y537S, or K303R ER alpha.

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Genome-wide analysis of transposase-accessible chromatin regions of MDA-MB-453 cells expressing ectopic wild-type, Y537S, or K303R ER alpha.

Project description:Genome-wide analysis of transposase-accessible chromatin regions of MDA-MB-453 cells expressing ectopic wild-type, Y537S, or K303R ER alpha.

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Genome-wide analysis of ectopically expressed wild-type, Y537S, or K303R ER alpha-binding genomic regions in MDA-MB-453 cells.

Project description:We analyzed the wild-type, Y537S, or K303R ER alpha-binding genomic regions ectopically expressed in MDA-MB-453 cells by ChIP-seq, and identified K303R-related disordered ERa binding and chromatin opening at Fox motif regions.

2022-12-16 | GSE191058 | GEO

Breast cancer cell line MDA-MB-453 response to DHT

Project description:This SuperSeries is composed of the following subset Series: GSE28305: Effect of 5a-dihydrotestosterone on breast cancer cell line MDA-MB-453 GSE28788: Androgen receptor cistrome in breast cancer cell line MDA-MB-453 with 5a-dihydrotestosterone (DHT) stimulation Refer to individual Series

| S-ECPF-GEOD-28789 | biostudies-other

Multifunctional Cu<sub>2-x</sub>Te Nanocubes Mediated Combination Therapy for Multi-Drug Resistant MDA MB 453.

Project description:Hypermethylated cancer populations are hard to treat due to their enhanced chemo-resistance, characterized by aberrant methylated DNA subunits. Herein, we report on invoking response from such a cancer lineage to chemotherapy utilizing multifunctional copper telluride (Cu2-XTe) nanocubes (NCs) as photothermal and photodynamic agents, leading to significant anticancer activity. The NCs additionally possessed photoacoustic and X-ray contrast imaging abilities that could serve in image-guided therapeutic studies.

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Effect of 5a-dihydrotestosterone on breast cancer cell line MDA-MB-453

Project description:Analysis of MDA-MB-453 breast cancer cells treated with the androgen 5a-dihydrotestosterone (DHT) for 6h, 16h and 48h to define the genes that are differentially regulated in response to DHT. MDA-MB-453 breast cancer cells were treated with 5a-dihydrotestosterone (DHT) for time course, followed by RNA extraction and hybridization on Affymetrix microarrays, in order to obtain the gene expression profiles at three time points. The vehicle treated samples are used as control.

| S-ECPF-GEOD-28305 | biostudies-other

CX3CL1 Overexpression Prevents the Formation of Lung Metastases in Trastuzumab-Treated MDA-MB-453-Based Humanized Tumor Mice (HTM).

Project description:CX3CL1 is a multifunctional chemokine that is involved in numerous biological processes, such as immune cell attraction and enhanced tumor immune cell interaction, but also in enhancing tumor cell proliferation and metastasis. The multifarious activity is partially determined by two CX3CL1 isoforms, a membrane-bound and a soluble version generated by proteolytic cleavage through proteases. Here, we investigated the impact of CX3CL1 overexpression in MDA-MB-453 and SK-BR-3 breast cancer cells. Moreover, we evaluated the therapeutic capacity of Matrix-Metalloproteinases-inhibitors TMI-1 and GI254023X in combination with the anti-HER2 antibody trastuzumab in vitro and in vivo. TMI-1 and GI254023X caused a reduced shedding of CX3CL1 and of HER2 in vitro but without effects on tumor cell proliferation or viability. In addition, trastuzumab treatment did not retard MDA-MB-453 cell expansion in vitro unless CX3CL1 was overexpressed upon transfection (MDA-MB-453CX3CL1). In humanized tumor mice, which show a coexistence of human tumor and human immune system, CX3CL1 overexpression resulted in a slightly enhanced tumor growth. However, trastuzumab treatment attenuated tumor growth of both MDA-MB-453CX3CL1 and empty vector transfected MDA-MB-453 transplanted mice but showed enhanced efficiency especially in preventing lung metastases in CX3CL1 overexpressing cancer cells. However, TMI-1 did not further enhance the trastuzumab treatment efficacy.

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Estrogen-independent Myc overexpression confers endocrine therapy resistance on breast cancer cells expressing ER?Y537S and ER?D538G mutations.

Project description:Approximately 30% of metastatic breast cancers harbor estrogen receptor ? (ER?) mutations associated with resistance to endocrine therapy and reduced survival. Consistent with their constitutive proliferation, T47D and MCF7 cells in which wild-type ER? is replaced by the most common mutations, ER?Y537S and ER?D538G, exhibit partially estrogen-independent gene expression. A novel invasion/dissociation/rebinding assay demonstrated that the mutant cells have a higher tendency to dissociate from invasion sites and rebind to a second site. Compared to ER?D538G breast tumors, ER?Y537S tumors exhibited a dramatic increase in lung metastasis. Transcriptome analysis showed that the ER?Y537S and ER?D538G mutations each elicit a unique gene expression profile. Gene set enrichment analysis showed Myc target pathways are highly induced in mutant cells. Moreover, chromatin immunoprecipitation showed constitutive, fulvestrant-resistant, recruitment of ER? mutants to the Myc enhancer region, resulting in estrogen-independent Myc overexpression in mutant cells and tumors. Knockdown and virus transduction showed Myc is necessary and sufficient for ligand-independent proliferation of the mutant cells but had no effect on metastasis-related phenotypes. Thus, Myc plays a key role in aggressive proliferation-related phenotypes exhibited by breast cancer cells expressing ER? mutations.

| S-EPMC6351074 | biostudies-literature

AR heterogeneity in TNBC MDA-MB-453 cells

Project description:Triple-negative breast cancer (TNBC) is aggressive and difficult, and few targeted therapies are available to treat this patient population. The androgen receptor (AR) has emerged as a potential target in breast cancer. Newer generation AR inhibitors, such as Seviteronel (Sevi), are unique in their ability to inhibit AR both directly and by blocking upstream androgen synthesis. The purpose of this study was to investigate the pre-clinical activity of Sevi in TNBC and further explore the effectiveness of targeting both androgen biosynthesis and AR activity in combination with other downstream acting agents. AR overexpressing (AR+) TNBC cell lines, xenografts and androgen responsive patient-derived xenograft (PDX) models were using to show how effectively Sevi inhibits AR activity and cell/tumor proliferation. Single cell RNA-sequencing of the AR+ cell line MDA-MB-453 illustrated heterogeneity in AR levels and identified cell cycle pathway activation in ARHigh versus ARLow expressing cells. Combination treatment with the cell cycle CDK4/6 inhibitor abemaciclib and Sevi showed synergy in AR+ TNBC cells and increased effectiveness, compared to each drug alone, in an AR+ TNBC xenograft model. While cell cycle inhibitors have been approved for use in hormone-receptor positive breast cancer, our studies suggest that these drugs may be equally effective in AR+ TNBC cells, especially when combined with AR antagonists. Implications. These data suggest that targeting AR signaling at multiple points throughout the pathway may be an effective was to treat patients with AR+ TNBC.

2020-06-12 | GSE152315 | GEO

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