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Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE113687 | GEO | 2020/08/18

REPOSITORIES: GEO

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Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer. [RNA-Seq2]

Project description:Purpose:Assess the difference in gene expression of taxol-resistant TNBC cells relative to parental cells (MDA-MB-436 and HS 578t) Methods: RNA-seq was performed on paclitaxel-treated MDA-MB-436 cells that are resistant to Paclitaxel (R20A, R20B, R20C) and in control-treated (DMSO) parental MDA-MB-436 cells that are sensitive to Paclitaxel (DMSO) Results: We mapped about 20 million sequence reads per sample to the human genome (hg19) and identified identified differentially expressed genes Conclusions: Our study identified genes significantly enriched or repressed in taxol-resistant cells relative to parental cells in both TNBC models (MDA_MB-436 and HS 578T)

2020-08-18 | GSE113685 | GEO

Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer. [ChIP-Seq]

Project description:Purpose:Assess the reprogramming of H3K4me1, H3K4me3, H3K27ac and H3K27me3 in paclitaxel-resistant triple-negative breast cancer cells relative to paclitaxel-sensitive cells Methods: ChIP-seq was performed on paclitaxel-treated MDA-MB-436 cells that are resistant to Paclitaxel (R20A, R20B, R20C) and in control-treated (DMSO) parental MDA-MB-436 cells that are sensitive to Paclitaxel (DMSO) Results: Using we mapped about 20 million sequence reads per sample to the human genome (hg19) and identified significant peaks in each cell lines using MACS.2.0 tool. Conclusions: Our study identified major reprogramming of H3K27me3 in the taxol-resistant TNBC cells relative to parental (TNBC cells), with loss of discrete H3K27me3 peaks in the resistant cells concomittent to acquisition of clusters of H3K27me3.

2020-08-18 | GSE113684 | GEO

Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer. [RNA-Seq1]

Project description:Purpose:Assess the difference in gene expression of taxol-resistant TNBC cells relative to parental cells (MDA-MB-436 and HS 578T) upon treatment with UNC1999 3uM Conclusions: Our study identified genes significantly enriched or repressed in taxol-resistant cells relative to parental cells in both TNBC models (MDA_MB-436 and HS 578T)

2020-08-18 | GSE111920 | GEO

Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer [Methylation profiling]

Project description:Purpose: Assess the difference in DNA methylation of taxol-resistant TNBC cells relative to parental cells (MDA-MB-436)

2020-08-18 | GSE111541 | GEO

Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer

Project description:Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer

| PRJNA453605 | ENA

Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer. [RNA-Seq1]

Project description:Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer. [RNA-Seq1]

| PRJNA438543 | ENA

Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer. [RNA-Seq2]

Project description:Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer. [RNA-Seq2]

| PRJNA453601 | ENA

Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer [Methylation profiling]

Project description:Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer [Methylation profiling]

| PRJNA437322 | ENA

Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer. [ChIP-Seq]

Project description:Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer. [ChIP-Seq]

| PRJNA453603 | ENA

Omics Analysis of Chemoresistant Triple Negative Breast Cancer Cells Reveals Novel Metabolic Vulnerabilities.

Project description:The emergence of drug resistance in cancer poses the greatest hurdle for successful therapeutic results and is associated with most cancer deaths. In triple negative breast cancer (TNBC), due to the lack of specific therapeutic targets, systemic chemotherapy is at the forefront of treatments, but it only benefits a fraction of patients because of the development of resistance. Cancer cells may possess an innate resistance to chemotherapeutic agents or develop new mechanisms of acquired resistance after long-term drug exposure. Such mechanisms involve an interplay between genetic, epigenetic and metabolic alterations that enable cancer cells to evade therapy. In this work, we generated and characterized a chemoresistant TNBC cell line to be used for the investigation of mechanisms that drive resistance to paclitaxel. Transcriptomic analysis highlighted the important role of metabolic-associated pathways in the resistant cells, prompting us to employ 1H-NMR to explore the metabolome and lipidome of these cells. We identified and described herein numerous metabolites and lipids that were significantly altered in the resistant cells. Integrated analysis of our omics data revealed MSMO1, an intermediate enzyme of cholesterol biosynthesis, as a novel mediator of chemoresistance in TNBC. Overall, our data provide a critical insight into the metabolic adaptations that accompany acquired resistance in TNBC and pinpoint potential new targets.

| S-EPMC9454761 | biostudies-literature

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