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

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

PROVIDER: PRJNA438543 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6845210_1.fastq.gz	Fastqsanger.gz
	SRR6845210_2.fastq.gz	Fastqsanger.gz
	SRR6845220_1.fastq.gz	Fastqsanger.gz
	SRR6845220_2.fastq.gz	Fastqsanger.gz
	SRR6845211_1.fastq.gz	Fastqsanger.gz

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Metabolic adaptations underlie epigenetic vulnerabilities in chemoresistant breast cancer

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

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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)

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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.

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