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

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

PROVIDER: PRJNA453601 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7064970_1.fastq.gz	Fastqsanger.gz
	SRR7064970_2.fastq.gz	Fastqsanger.gz
	SRR7064980_1.fastq.gz	Fastqsanger.gz
	SRR7064980_2.fastq.gz	Fastqsanger.gz
	SRR7064990_1.fastq.gz	Fastqsanger.gz

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Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer

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

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

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

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

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

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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

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-08-18 | GSE113687 | 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

Bioenergetic Adaptations in Chemoresistant Ovarian Cancer Cells.

Project description:Earlier investigations have revealed that tumor cells undergo metabolic reprogramming and mainly derive their cellular energy from aerobic glycolysis rather than oxidative phosphorylation even in the presence of oxygen. However, recent studies have shown that certain cancer cells display increased oxidative phosphorylation or high metabolically active phenotype. Cellular bioenergetic profiling of 13 established and 12 patient derived ovarian cancer cell lines revealed significant bioenergetics diversity. The bioenergetics phenotype of ovarian cancer cell lines correlated with functional phenotypes of doubling time and oxidative stress. Interestingly, chemosensitive cancer cell lines (A2780 and PEO1) displayed a glycolytic phenotype while their chemoresistant counterparts (C200 and PEO4) exhibited a high metabolically active phenotype with the ability to switch between oxidative phosphorylation or glycolysis. The chemosensitive cancer cells could not survive glucose deprivation, while the chemoresistant cells displayed adaptability. In the patient derived ovarian cancer cells, a similar correlation was observed between a high metabolically active phenotype and chemoresistance. Thus, ovarian cancer cells seem to display heterogeneity in using glycolysis or oxidative phosphorylation as an energy source. The flexibility in using different energy pathways may indicate a survival adaptation to achieve a higher 'cellular fitness' that may be also associated with chemoresistance.

| S-EPMC5562731 | biostudies-literature

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