Genome-wide H3k27ac levels following FOXA1 KO in UMUC-1 human bladder cancer cells [RNA-seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE172432 | GEO | 2022/09/08
REPOSITORIES: GEO
Similar Datasets
Project description:We report areas of H3K27ac modification in both wild-type (parental) UMUC-1 and UMUC-1 FOXA1 KO bladder cancer cells.
2022-09-08 | GSE172431 | GEO
Project description:10x scRNA-Seq results of a bladder cancer case with extensive squamous cell differentation
2022-09-08 | GSE176249 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-09-08 | GSE172433 | GEO
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.
2014-08-01 | E-GEOD-56037 | biostudies-arrayexpress
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.
2016-06-30 | E-MTAB-4089 | biostudies-arrayexpress
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 3’UTR 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.
2014-08-01 | GSE56037 | GEO
Project description:Gene expression profiles (RNA seq of parental MCF7 cells and tamoxifen resistant cells after ER or FOXA1 knock down and after overexpression of FOXA1 in parenatl cells).
2016-11-01 | GSE75329 | GEO
Project description:Consistent with the previous study, we showed that tumor molecular subtypes switched between the luminal subtype and the basal subtype during long-term maintenance of conventional tumor organoids in the absence of stroma in vitro, indicating the important role of tumor stroma in maintaining the tumor phenotype. Interestingly, genomic alterations seen in parental tumors are preserved well in both conventional tumor organoids and tumor assembloids, implying that the determination of tumor phenotypes may rely on epigenetic changes in tumor stroma-dependent ways, particularly through stromal BMP signals, elicited by Hh expression in tumor cells. We performed extensive epigenomic analyses including RNA-seq, ATAC-seq, and ChIP-seq with genetically manipulated tumor assembloids, in which genetic manipulations were applied independently to tumor organoids and tumor stroma in a combinatorial manner. Using this system, we identified FOXA1 as a master pioneering factor that drives enhancer reprogramming during the molecular switching of tumor subtypes. We have also obtained new evidence that FOXA1 is induced by stromal BMP signals and identified the HH-BMP-FOXA1 signaling feedback between urothelial tumors and stromal fibroblasts as a critical signaling axis in the FOXA1-mediated enhancer reprogramming of tumor phenotypes in the determination of urothelial carcinomas.
2020-09-27 | GSE148819 | GEO
Project description:Exclusion of lymphocytes from tumors is a major barrier for effective immuno- and chemo-therapy of cancer. We found that FOXA1 overexpression inversely correlates with expression of antigen processing and presentation and interferon signaling genes in different cancer types. FOXA1 binds to STAT proteins and inhibits expression of antigen presentation and interferon response genes and tumor immunity independent of the forkhead domain - DNA binding function. Increased FOXA1 also correlates with immunotherapy resistance in murine triple negative breast tumor and bladder cancer in patients and chemo-resistance in breast cancer patients. Our results reveal that FOXA1 is a key immune suppressor, suggesting that FOXA1 overexpression may predict tumor resistance to immuno- and chemo-therapies and that depletion of FOXA1 may therapeutically convert cancers from ‘immune-cold’ to ‘immune-hot’ diseases.
2020-12-31 | GSE142221 | GEO
Project description:We report the dual role of FoxA1 in androgen receptor recruitment to the chromatin of androgen responsive prostate cancer cell line LNCaP-1F5 using ChIP-sequencing. Depletion of FoxA1 reprograms both androgen and glucocorticoid receptor recruitment and subsequent gene expression. The ChIP-seq has been performed using AR, FoxA1, GR, H3K4me2 antibodies. We have also mapped the DNaseI-hypersensitive sites (DHS) using deep sequencing. LNCaP-1F5 cells were depleted of FoxA1 using siRNAs. Parental cells and FoxA1 depleted cells (siFoxA1) were treated with vehicle or 100 nM DHT or (100 nM DEX) for 24 hours followed by RNA isolation and hybridization to Illumina arrays. All the experiments have been performed in biological duplicates. Parental cells treated with DHT (or DEX) were analyzed for differentially expressed genes compared to vehicle treated parental cells. Similarly siFoxA1 cells treated with DHT (or DEX) were analyzed for differentially expressed genes compared to vehicle treated siFoxA1 cells.
2011-09-13 | E-GEOD-30622 | biostudies-arrayexpress