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Genome-wide RNA-seq from PARP1 and PRC2 double-depleted MDA-MB-231 cell lines

ABSTRACT: Genome-wide RNA-seq from PARP1 and PRC2 double-depleted MDA-MB-231 cell lines

PROVIDER: PRJNA598225 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10806593.fastq.gz	Fastqsanger.gz
	SRR10806594.fastq.gz	Fastqsanger.gz
	SRR10806595.fastq.gz	Fastqsanger.gz
	SRR10806596.fastq.gz	Fastqsanger.gz
	SRR10806597.fastq.gz	Fastqsanger.gz

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Genome-wide RNA-seq from PARP1 and PRC2 double-depleted MDA-MB-231 cell lines

Project description:Purpose: To identify downstream signaling pathways mediated by PARP1 and PRC2 in breast cancer Methods: RNAs isolated from MDA-MB-231 cells depleting PARP1 and EZH2 (PARP1 KO shEZH2) and PARP1 and SUZ12 (PARP1 KO shSUZ12) were analyzed by using an Illumina Nextseq500 Conclusions: Our study represents the first transcriptomic profiles of effects of PARP1 and PRC2 double deficiency in breast cancer

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Project description:Despite advances in cancer therapy, drug resistance remains a major obstacle in a range of cancer types, often driven by overexpression of ATP-binding cassette (ABC) transporters that restrict intracellular drug accumulation. Our previous studies identified the BRG1-p300 transcriptional complex at the promoters of specific ABC transporter genes. We used basal and induced doxorubicin-resistant triple-negative breast cancer (TNBC) cell lines to analyze changes in ABC transporter expression and drug accumulation following PARP1 inhibition. Moreover, the effect of commonly used antioxidants on the repressive effect of Veliparib against ABC genes was verified. ChIP-Seq was performed to identify transcription factor mediating PARP1-dependent ABC gene regulation. PARP1 inhibition or silencing of PARP1/HPF1 complex components downregulated ABCC and ABCG2 transporters, leading to increased intracellular accumulation of chemotherapeutic drugs in doxorubicin-resistant cells. Notably, suppression of genotoxic stress via antioxidant treatment reverses the inhibitory effect of Veliparib on ABC transporter expression. We identified SMARCA1 as a key regulator of PARP1-dependent expression of ABCC genes. SMARCA1 is a key effector of PARP1/p300-mediated regulation of ABC transporters and represents a potential therapeutic target in doxorubicin-resistant TNBC. These findings support the development of combinatorial strategies involving PARP1 inhibitors and chromatin remodeling modulators in refractory breast cancers.

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PRMT6 and PARP1 sequencing in non-treated MDA-MB-231 cells

Project description:PRMT6 and PARP1 sequencing in non-treated MDA-MB-231 cells

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PRMT6 and PARP1 sequencing in non-treated MDA-MB-231 cells

Project description:Here, we examined the interactions between PRMT6, poly(ADP-ribose) polymerase 1 (PARP1), and the cullin 4 B (CUL4B)-Ring E3 ligase (CRL4B) complex, to form a transcription-repressive complex that co-occupies the core clock gene PER3 promoter.

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Project description:RNA sequencing of GLO1-depleted MDA-MB-231 breast cancer cells

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The miRNA profiling in MDA-MB-231, MDA-MB-231/E1A and knockdown of Dicer in MDA-MB-231/E1A cells

Project description:Dicer, RNase III endonuclease, is an essential enzyme in miRNA biogenesis that regulates target gene expression, and it has been reported that aberrant expressions of Dicer associate with the clinical outcomes of patients in various cancers. To explore the miRNA differencial expression regulated by Dicer in MDA-MB-231/E1A cells, the microarray profiling analysis was employed to conduct differentially expressed miRNAs in stable MDA-MB-231/vector, MDA-MB-231/E1A, and MDA-MB-231/E1A/shDicer cells.

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The miRNA profiling in MDA-MB-231, MDA-MB-231/E1A and knockdown of Dicer in MDA-MB-231/E1A cells

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Expression profiles of MDA-MB-231, MDA-231 S1a and S1b

Project description:Identification of genes that are involved in self-seeding by comparing gene expression profiles between parental MDA-MB-231 cells and seeder cells (MDA-231-S1a and S1b) 2 replicates from each sample (parental MDA-MB-231, MDA-MB-231 S1a and MDA-MB-231 S1b) were analyzed

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Project description:Identification of genes that are involved in self-seeding by comparing gene expression profiles between parental MDA-MB-231 cells and seeder cells (MDA-231-S1a and S1b)

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