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Identification of PRMT5-dependent genes in ESA+CD24lowCD44+ MCF7 cells

ABSTRACT: Identification of PRMT5-dependent genes in ESA+CD24lowCD44+ MCF7 cells

PROVIDER: PRJNA421322 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6353800_1.fastq.gz	Fastqsanger.gz
	SRR6353800_2.fastq.gz	Fastqsanger.gz
	SRR6353795_1.fastq.gz	Fastqsanger.gz
	SRR6353795_2.fastq.gz	Fastqsanger.gz
	SRR6353796_1.fastq.gz	Fastqsanger.gz

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Identification of PRMT5-dependent genes in ESA+CD24lowCD44+ MCF7 cells

Project description:PRMT5 has been associated with poor prognosis in breast cancer. Here, we identify genes which are dependent on PRMT5 expression in MCF7 ESA+CD24lowCD44+ breast cancer stem cells by RNA-seq

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Identification of genes differentially expressed between breast cancer cell lines MCF7-TWIST1 and MCF7-Ctrl

Project description:Identification of genes differentially expressed between breast cancer cell lines MCF7-TWIST1 and MCF7-Ctrl

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PRMT5 knockdown changes gene expression in prostate cancer cells

Project description:PRMT5 is the major type II protein arginine methyltransferase catalyzing the symmetric dimethylation of arginine. Recent reports have indicated that PRMT5 is overexpressed in multiple cancer types, including prostate. However, the exact contribution of PRMT5 to prostate tumorigenesis is unknown. To explore the functional role of PRMT5 in prostate cancer (PCa), we knocked down PRMT5 by lentiviral shRNAs in both AR-dependent LNCaP cells and AR-independent PC3 cells. Our data suggests that PRMT5 regulates PCa cell biology. To further identify PRMT5-regulated genes in PCa, we performed paired-end RNA-seq analysis in PC3 and LNCaP cells with or without PRMT5-knockdown.

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Identification of Lef1-dependent genes in zebrafish and mouse hypothalamus

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A PRMT5-ZNF326 axis mediates innate immune activation upon replication stress

Project description:DNA replication stress (RS) is a widespread phenomenon in carcinogenesis, causing genomic instability and extensive chromatin alterations. DNA damage leads to activation of innate immune signaling, but little is known about transcriptional regulators mediating such signaling upon RS. Using a chemical screen, we identified protein arginine methyltransferase 5 (PRMT5) as a key mediator of RS-dependent induction of interferon-stimulated genes (ISGs). This response is also associated with reactivation of endogenous retroviruses (ERVs). Using quantitative mass spectrometry, we identify proteins with PRMT5-dependent symmetric dimethylarginine (SDMA) modification induced upon RS. Among these, we show that PRMT5 targets and modulates the activity of ZNF326, a zinc finger protein essential for ISG response. Our data demonstrate a role for PRMT5-mediated SDMA in the context of RS-induced transcriptional induction, affecting physiological homeostasis and cancer therapy.

2024-10-08 | PXD046082 | Pride

RNA-seq analysis of PRMT5-regulated genes in irradiated/non-irradiated LNCaP cells

Project description:DNA Double-strand break (DSB) repair is critical for cell survival and genome integrity. Upon recognition of DSBs, repair proteins are transiently upregulated to facilitate repair through homologous recombination (HR) or non-homologous end joining (NHEJ). We present evidence that PRMT5 cooperates with pICln to function as a master epigenetic activator of DNA damage response (DDR) genes involved in HR, NHEJ, and G2 arrest (including RAD51, BRCA1, and BRCA2) to upregulate gene expression upon DNA damage. Contrary to the predominant role of PRMT5 as an epigenetic repressor, our results demonstrate that PRMT5 and pICln can activate gene expression, potentially independent of PRMT5’s obligate cofactor MEP50. Targeting PRMT5 or pICln hinders repair of DSBs in multiple cancer cell lines, and both PRMT5 and pICln expression positively correlates with DDR genes across 32 clinical cancer data sets. Thus, targeting PRMT5 or pICln may be explored in combination with radiation or chemotherapy for cancer treatment.

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Identification of genes differentially expressed between breast cancer cell lines MCF7-TWIST1 and MCF7-Ctrl

Project description:In this study, we aimed to characterize the stimulatory role of TWIST1 in breast cancer cell proliferation, EMT and metastasis, uncover the underlying molecular mechanism, and identify potential therapeutic targets for treating BLBC. RNA-Seq analysis were performed to identify differentially expressed genes influenced by TWIST1 overexpression in breast cancer cell MCF7. Pathway enrichment analysis and gene set enrichment analysis were performed to identify TWIST1-regulated signaling pathways, particually the cancer-associated pathways. ChIP-Seq analysis was further performed to identify TWIST1-associated genomic regions in MCF7-TWIST1 cells. The potential direct target genes of TWIST1 were identified by combined analysis of the gene expression profiling data and ChIP-Seq data.

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