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Effect of SAT1 depletion on H3K27ac alterations in the ovarian cancer cell line SKOV3 in detached conditions by chromatin immunoprecipitation and sequencing (ChIP-seq) analysis

ABSTRACT: Effect of SAT1 depletion on H3K27ac alterations in the ovarian cancer cell line SKOV3 in detached conditions by chromatin immunoprecipitation and sequencing (ChIP-seq) analysis

PROVIDER: PRJNA1112431 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29060213_1.fastq.gz	Fastqsanger.gz
	SRR29060213_2.fastq.gz	Fastqsanger.gz
	SRR29060214_1.fastq.gz	Fastqsanger.gz
	SRR29060214_2.fastq.gz	Fastqsanger.gz
	SRR29060215_1.fastq.gz	Fastqsanger.gz

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Effect of SAT1 depletion on H3K27ac alterations in the ovarian cancer cell line SKOV3 in detached conditions by chromatin immunoprecipitation and sequencing (ChIP-seq) analysis

Project description:Ovarian cancer is an aggressive malignancy characterized by the ascitic fluid and peritoneal metastases. Cancer cells detach from the extracellular matrix and survives the loss of anchorage in the ascites to disseminate extensively in the peritoneal cavity. Metabolic reprogramming is often observed in the cancer progression, yet its role in peritoneal metastasis is largely unexplored. Here we report that spermidine/spermine N1-acetyltransferase 1 (SAT1) promotes the anchorage-independent cell survival and potentiates metastatic dissemination. Analysis of different histone modifications in the SAT1-depleted ovarian cancer cells upon detachment revealed only a dramatic reduction in the level of H3K27ac, whereas the levels of 15 other histone lysine modifications were not reduced or slightly affected. Chromatin immunoprecipitation and sequencing (ChIP-seq) analysis of H3K27ac to map gene regions with significantly altered H3K27ac identified 1870 genes with increased and 1556 genes with reduced H3K27ac peaks in SAT1-deficient ovarian cancer cells compared to control cells upon detachment.Integrated analysis of RNA-seq and H3K27ac ChIP-seq datasets indicated that 11.05% of genes with reduced H3K27ac peaks were transcriptionally down-regulated. Remarkably, such genes were broadly associated with mitotic cell cycle process, chromosome organization, and chromosome segregation.Taking these findings together, we conclude that SAT1 increases H3K27ac mark within genes required for mitosis regulation and chromosome segregation, thereby protecting ovarian cancer cells from mitotic catastrophe upon detachment.

2024-07-29 | GSE267703 | GEO

Effect of detachment culture condition and depletion of SAT1 on gene expression in SKOV3 ovarian cancer cell line

Project description:Ovarian cancer is an aggressive malignancy characterized by the ascitic fluid and peritoneal metastases. Cancer cells detach from the extracellular matrix and survives the loss of anchorage in the ascites to disseminate extensively in the peritoneal cavity. Metabolic reprogramming is often observed in the cancer progression, yet its role in peritoneal metastasis is largely unexplored. Here we report that spermidine/spermine N1-acetyltransferase 1 (SAT1) promotes the anchorage-independent cell survival and potentiates metastatic dissemination. We compared the detached vs attached cells with RNAseq and identified that hypoxia was among the most enriched pathways using gene set enrichment analysis.To define the underlying mechanism, we first carried out RNA-seq analysis of the detached ovarian cancer cells with or without knocking down SAT1 and identified 1,829 differentially expressed genes (P value < 0.05) in the detached SAT1 knocking down cells. Gene Ontology (GO) term enrichment analysis recognized the differentially expressed genes associated extensively with mitotic process, most likely reflecting a role of SAT1 in cell cycle control. Taken together, our data suggest that SAT1 was induced by hypoxia in the detached cell and played an important role in cell cycle control.

2024-07-29 | GSE267614 | GEO

H3K27ac, H3K4me3, H3K27me3 and H3K9me3 ChIPseq of SKOV3(AA) and SKOV3(CC)

Project description:To study the effect of rs1192691 on histone modifications, we performed H3K27ac, H3K4me3, H3K27me3 and H3K9me3 in SKOV3(AA) and SKOV3(CC).

2022-01-18 | GSE182333 | GEO

EZH2 and H3K27ac ChIPseq of SKOV3(AA) and SKOV3(CC)

Project description:EZH2 and H3K27ac ChIPseq of SKOV3(AA) and SKOV3(CC)

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H3K27ac, H3K4me3, H3K27me3 and H3K9me3 ChIPseq of SKOV3(AA) and SKOV3(CC)

Project description:H3K27ac, H3K4me3, H3K27me3 and H3K9me3 ChIPseq of SKOV3(AA) and SKOV3(CC)

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Identification of SAT1 regulated genes in GBM cells by microarray

Project description:We aimed to identify SAT1 regulated genes in U87MG cell by knockdown of SAT1 with two different shRNAs, and then compared knockdown cells to control cells with shGFP

2021-06-23 | GSE116395 | GEO

Effects of deletion of SAT1, a polyamine-metabolic enzyme, on mouse HeLa xenograft tumor

Project description:An acidic tumor microenvironment plays a critical role in tumor progression. However, understanding of metabolic reprogramming of tumors in response to acidic extracellular pH has remained elusive. Using comprehensive metabolomic analyses, we demonstrated that acidic extracellular pH (pH 6.8) leads to the accumulation of N1-acetylspermidine, a pro-tumor metabolite, through upregulation of the expression of spermidine/spermine acetyl transferase 1 (SAT1). Inhibition of SAT1 expression suppressed the accumulation of intra- and extracellular N1-acetylspermidine at acidic pH. Conversely, overexpression 3 of SAT1 increased intra- and extracellular N1-acetylspermidine levels, supporting the proposal that SAT1 is responsible for accumulation of N1-acetylspermidine. While inhibition of SAT1 expression only had a minor effect on cancer cell growth in vitro, SAT1 knockdown significantly decreased tumor growth in vivo, supporting a contribution of the SAT1-N1-acetylspermidine axis to pro-tumor immunity. Immune cell profiling revealed that inhibition of SAT1 expression decreased neutrophil recruitment to the tumor, resulting in impaired angiogenesis and tumor growth. We showed that anti-neutrophil neutralizing antibodies suppressed growth in control tumors to a similar extent to that seen in SAT1 knockdown tumors in vivo. Further, a SAT1 signature was found to be correlated with poor patient prognosis. Our findings demonstrate that extracellular acidity stimulates recruitment of pro-tumor neutrophils via the SAT1-N1-acetylspermidine axis, which may represent a novel target for anti-tumor immune therapy.

2023-08-14 | GSE239784 | GEO

Genes regulated by SAT1 in brain tumors

Project description:Performed gene expression profiling of U87MG cells with two different shRNAs to SAT1 using Affymetrix microarrays covering 67,528 gene transcripts. Accordingly, we infected U87MG cells with lentiviruses expressing shRNAs to either the green fluorescent protein (GFP) or SAT1, performed a drug selection to ensure stable expression of the shRNAs, and expanded the cells for RNA harvest within 7 days of infection. RNA was reverse transcribed into cDNA, labelled with biotin and hybridized onto the arrays for analyses. Hierarchical clustering of duplicate experiments correctly segregated samples according to sample identity (i.e. shGFP clustered together, shSAT1-1 clustered together, and shSAT1-2 clustered together; with the latter two separately branching from shGFP)

2019-09-18 | E-MTAB-7270 | biostudies-arrayexpress

RNAseq of SKOV3(AA) and SKOV3(CC)

Project description:To study the effect of rs1192691 on ovarian cancer cells, we generated SKOV3(CC) from SKOV3(A/A) using CRISPR/Cas9 technology and performed RNA-seq.

2022-01-18 | GSE181884 | GEO

RNAseq of SKOV3(AA) and SKOV3(CC)

Project description:RNAseq of SKOV3(AA) and SKOV3(CC)

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