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Genome-wide H3k27ac levels following FOXA1 KO in UMUC-1 human bladder cancer cells

ABSTRACT: Genome-wide H3k27ac levels following FOXA1 KO in UMUC-1 human bladder cancer cells

PROVIDER: PRJNA723297 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR14286562.fastq.gz	Fastqsanger.gz
	SRR14286563.fastq.gz	Fastqsanger.gz
	SRR14286564.fastq.gz	Fastqsanger.gz
	SRR14286565.fastq.gz	Fastqsanger.gz

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Genome-wide H3k27ac levels following FOXA1 KO in UMUC-1 human bladder cancer cells [RNA-seq]

Project description:We report areas of H3K27ac modification in both wild-type (parental) UMUC-1 and UMUC-1 FOXA1 KO bladder cancer cells.

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Genome-wide H3k27ac levels following FOXA1 KO in UMUC-1 human bladder cancer cells [ChIP-seq]

Project description:We report areas of H3K27ac modification in both wild-type (parental) UMUC-1 and UMUC-1 FOXA1 KO bladder cancer cells.

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Genome-wide H3k27ac levels following FOXA1 KO in UMUC-1 human bladder cancer cells [ChIP-seq]

Project description:Genome-wide H3k27ac levels following FOXA1 KO in UMUC-1 human bladder cancer cells [ChIP-seq]

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Genome-wide H3k27ac levels following FOXA1 KO in UMUC-1 human bladder cancer cells [RNA-seq]

Project description:Genome-wide H3k27ac levels following FOXA1 KO in UMUC-1 human bladder cancer cells [RNA-seq]

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Genome-wide H3k27ac levels following FOXA1 KO in UMUC-1 human bladder cancer cells [scRNA-Seq]

Project description:Genome-wide H3k27ac levels following FOXA1 KO in UMUC-1 human bladder cancer cells [scRNA-Seq]

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Genome-wide H3k27ac levels following FOXA1 KO in UMUC-1 human bladder cancer cells [scRNA-Seq]

Project description:10x scRNA-Seq results of a bladder cancer case with extensive squamous cell differentation

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Genome-wide H3k27ac levels following FOXA1 KO in UMUC-1 human bladder cancer cells

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

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Gene expression data from UMUC-14 following FGFR3 knock-down using FGFR3 siRNAs

Project description:To better understand the molecular mechanisms underlying altered-FGFR3 oncogenic activity in bladder carcinomas, we made use of UMUC-14 cell lines, which endogenously expressed a mutated activated form of FGFR3 (FGFR3-S249C), the growth and transformation of these cell lines being dependent on activated-FGFR3 activity. We conducted a gene expression analysis using Affymetrix DNA arrays in this cell line treated or not with FGFR3 siRNAs.

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Project description:We profiled the genome-wide occupancy of three tissue-specific transcription factors, HNF4A, CEBPA and FOXA1, as well as the genome-wide occurrence of the histone mark, H3K4me3 in the livers of two inbred parental mouse strains (C57BL/6J and CAST/EiJ) and their F1 crosses. We also included H3K27ac data generated from F1 hybrids as well as the profiling of HNF4A, CEBPA and FOXA1 in both CEBPA and HNF4a heterozygous knock-outs.

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Effect of increased FOXA1 on gene expression in bladder cancer cells

Project description:Urothelial cell carcinoma of the bladder (UCC) is a common disease characterized by FGFR3 mutation. Whilst upregulation of this oncogene occurs most frequently in low-grade non-invasive tumors, recent data reveal increased FGFR3 expression characterizes a common sub-type of invasive UCC sharing genetic similarities with lobular breast cancer. These similarities include upregulation of the FOXA1 transcription factor and reduced expression of microRNAs-99a/100. We have previously identified direct regulation of FGFR3 by these two microRNAs and now search for further targets. Using a microarray meta-database we find potential FOXA1 regulation by microRNAs-99a/100. We confirm direct targeting of the FOXA1 3âUTR by microRNAs-99a/100 and also potential indirect regulation through microRNA-485-5p/SOX5/JUN-D/FOXL1 and microRNA-486/FOXO1a. In 292 benign and malignant urothelial samples, we find an inverse correlation between the expression of FOXA1 and microRNAs-99a/100 (r=-0.33 to -0.43, p<0.05). As for FGFR3 in UCC, tumors with high FOXA1 expression have lower rates of progression than those with low expression (Log rank p=0.009). Using global gene expression and CpG methylation profiling we find genotypic consequences of FOXA1 upregulation in UCC. These are associated with regional hypomethylation and near FOXA1 binding sites, and mirror patterns previously reported in FGFR3 mutant UCC. These include gene silencing through aberrant hypermethylation (e.g. IGFBP3) and affect genes that characterize lobular breast cancer (e.g. ERBB2, XBP1). In conclusion, we have identified microRNAs-99a/100 mediate a direct relationship between FGFR3 and FOXA1, and potentially facilitate cross talk between these pathways in UCC. Gene expression profiling of EJ Bladder cancer cells transfected with FOXA1 construct or with empty pUC19 vector.

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