Whole-genome sequencing of nine esophageal adenocarcinoma cell lines.
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB14018 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| OACM5.1.snp.pass.vcf.gz | Vcf | |||
| OACM5.1.snp.pass.vcf.gz.tbi | Vcf | |||
| FLOW.snp.pass.vcf.gz | Vcf | |||
| FLOW.snp.pass.vcf.gz.tbi | Vcf | |||
| SKGT4.snp.pass.vcf.gz | Vcf |
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Project description:rna sequencing of Oesophageal Adenocarcinoma Cell lines: OACP4, OE19, FLO-1, SK-GT-4, ESO26, OE33, ESO51, OACM5.1 C, JH-EsoAd1
2022-06-01 | GSE153096 | GEO
Project description:A nonsense mutation in ARID1A was identified by next generation sequencing in non-dysplastic Barrett's esophagus [BE] tissue and esophageal adenocarcinoma [EAC] tissue of a patient diagnosed with EAC. Immunohistochemistry performed on an independent archival cohort demonstrated ARID1A protein loss in 0% (0/76), 4.9% (2/40), 14.3% (4/28), 16.0% (8/50), and 12.2% (12/98) of normal squamous epithelium, BE, low-, high-grade dysplasia, and EAC tissues, respectively. Enhanced cell growth, proliferation and invasion were observed upon ARID1A knockdown in EAC cells. ARID1A was knocked down in OE33 cells (Sample MS_1 and MS_3) using on-TARGET smartpool ARID1A siRNA. At the same time, OE33 cells were transfected with a non-targeting siRNA, and these experiments (Samples MS_2 and MS_4) functioned as mock controls. Cells were harvested after 48 hours and total RNA was extracted using the Rneasy kit (Qiagen)
2012-06-01 | GSE38380 | GEO
Project description:A nonsense mutation in ARID1A was identified by next generation sequencing in non-dysplastic Barrett's esophagus [BE] tissue and esophageal adenocarcinoma [EAC] tissue of a patient diagnosed with EAC. Immunohistochemistry performed on an independent archival cohort demonstrated ARID1A protein loss in 0% (0/76), 4.9% (2/40), 14.3% (4/28), 16.0% (8/50), and 12.2% (12/98) of normal squamous epithelium, BE, low-, high-grade dysplasia, and EAC tissues, respectively. Enhanced cell growth, proliferation and invasion were observed upon ARID1A knockdown in EAC cells. ARID1A was knocked down in OE33 cells (Sample MS_1 and MS_3) using on-TARGET smartpool ARID1A siRNA. At the same time, OE33 cells were transfected with a non-targeting siRNA, and these experiments (Samples MS_2 and MS_4) functioned as mock controls. Cells were harvested after 48 hours and total RNA was extracted using the Rneasy kit (Qiagen) Aim Affymetrix Human PrimeView Gene Expression Array : to determine the downstream effectors of ARID1A that are likely to contribute to the oncogenic phenotype caused by ARID1A down-regulation. Two biological replicates of each condition (2x ARID1A knockdown, and 2x Mock) were used for the microarray experiment.
2012-05-31 | E-GEOD-38380 | biostudies-arrayexpress
Project description:Background & Aims: Alterations in methylation of protein-coding genes have been associated with development of Barrett’s esophagus (BE) and esophageal adenocarcinoma (EAC). Deregulation of non-coding RNAs has been associated with carcinogenesis, but never studied in BE or EAC cells. We used high-resolution methylome analysis to identify changes at genomic regions that encode non-coding RNAs in BE and EAC cells. Methods: We analyzed the methylation status of 1.8 million CpG sites using the massively parallel sequencing-based HELP-tagging assay in matched sets of BE and healthy esophageal tissues from the same patients. We also analyzed human EAC cell lines (OE-33, SK-GT-4, and FLO-1) and human primary non-immortalized esophageal epithelial cells (HEEpiC). Results: BE was characterized by genome-wide loss of methylation that significantly affected intragenic and repetitive elements of the genome. A high proportion of non-coding regions were hypomethylated in BE tissues. The changes in methylation affected small and long non-coding (lnc) regions, and discriminated healthy esophageal from BE tissues, even in matched samples. One lncRNA, AFAP1-AS1, was highly hypomethylated and overexpressed in EAC cells, compared with primary non-malignant esophageal epithelial cells. Knockdown of AFAP1-AS1 with small interfering RNA inhibited proliferation and colony-forming ability of EAC cells, inducing apoptosis; knockdown also significantly reduced EAC cell migration and invasion in Matrigel assays. Conclusions: BE tissues have reduced genome-wide methylation, compared with healthy esophageal tissues, that includes many non-coding regions. Methylation of the long noncoding RNA AFAP1-AS1 is reduced in EAC cells, increasing its expression and the aggressive behavior of cells in culture, similar to activation of protein-coding oncogenes.
2015-12-26 | GSE43150 | GEO
Project description:Esophageal Adenocarcinoma (EAC) is highly mutated and molecularly heterogeneous. The number of cell lines available for study is limited and their genome has been only partially characterized. The availability of an accurate annotation of their mutational landscape is crucial for accurate experimental design and correct interpretation of genotype-phenotype findings. We performed high coverage, paired end whole genome sequencing on eight EAC cell lines—ESO26, ESO51, FLO-1, JH-EsoAd1, OACM5.1 C, OACP4 C, OE33, SK-GT-4—all verified against original patient material, and one esophageal high grade dysplasia cell line, CP-D. We have made available the aligned sequence data and report single nucleotide variants (SNVs), small insertions and deletions (indels), and copy number alterations, identified by comparison with the human reference genome and known single nucleotide polymorphisms (SNPs). We compare these putative mutations to mutations found in primary tissue EAC samples, to inform the use of these cell lines as a model of EAC.
2016-07-19 | PRJEB14018 | EVA
Project description:We report the identification of FLO-1, and derivation of its isogenic companion FLO-1LM, as two spontaneously metastatic cell line models of human esophageal adenocarcinoma (EAC). We performed genome-wide RNAseq comparing FLO-1LM and FLO-1 parental cells to gain molecular insights into the phenotypic differences between these two cell lines. Using an adjusted p-value<0.05, a total of 375 (307 downregulated, 68 upregulated) genes were differentially regulated in FLO-1LM compared with parental cells. Genome-wide RNAseq profiling revealed significant enrichment of metastasis-related pathways in FLO-1LM cells, many of which are also evident in patient samples. Moreover, CDH1, which encodes the adhesion molecule E-cadherin, was the most significantly downregulated gene in FLO-1LM compared to FLO-1.
2016-10-18 | GSE88802 | GEO
Project description:RNA-seq was performed on esophageal adenocarcinoma (EAC), Barrett's without dysplasia, Barrett's with low-grade dysplasia (LGD) and normal squamous esophagus tissue to find early alterations in the transcriptome level turning Barrett's dysplastic.
2017-07-23 | E-MTAB-4054 | biostudies-arrayexpress
Project description:We identified FOXM1 as an EAC-specific candidate transcription factor using GSEA analysis. Functionality of FOXM1 was evaluated in both EAC patient derived organoids and EAC cell lines by measuring cell proliferation, colony formation, and xenograft growth. A FOXM1 signature through the overlap of ESO26, SKGT4, and OE33 intersected ChIP-seq peaks and ESO26 siFOXM1 RNA-seq downregulated genes. Upstream transcriptional regulation of FOXM1 was evaluated with this FOXM1 gene signature and validated using pharmacological inhibition. GSEA analysis determined that immune related pathways were upregulated in ESO26 cell lines treated with siFOXM1 or in TCGA EAC patients with low FOXM1 expression. Syngeneic xenografts found increases in CD8+ T cell infiltration in FOXM1 knockdown tumors. Loss of FOXM1 led to increased secretion of CD8+ T cell Th1 chemokines which play a role in the migration of CD8+ T cells upon loss of FOXM1. Finally, the loss of FOXM1 also increased Ex-vivo cytotoxic killing of murine cancer cells.
2024-02-28 | GSE236847 | GEO
Project description:Esophageal adenocarcinoma (EAC) is a highly aggressive malignancy that frequently develops from Barrettâs esophagus (BE), a premalignant pathological change occurring in the lower end of esophagus. To identify BE patients at high risk of malignant transformation is essential to the prevention of EAC. Although microRNA (miRNA) expression signatures have been associated with the etiology and prognosis of several types of cancers, their roles in the development of EAC have not been extensively evaluated. We analyzed the expression patterns of 470 human miRNAs using Agilent miRNA microarray in 32 disease/normal-paired tissues from 16 patients diagnosed with BE of either low or high grade dysplasia, or EAC
2010-05-16 | E-GEOD-16456 | biostudies-arrayexpress
Project description:Esophageal cancers (ECs) are highly aggressive tumors with poor prognosis and few treatment options. This study investigated the possibility of treating esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) cells by inhibitors of broad and specific histone deacetylases (HDACi; SAHA, MS-275, FK228) and/or of DNMT (Azacytidine, AZA). Drug targets (HDAC1,2,3 and DNMT1) were present in non-neoplastic (HET-1A), ESCC (OE21) and EAC (OE33) cell lines. All cell lines responded to HDACi by reduced HDAC activity and increased histone acetylation as well as to AZA by up-regulation of p21. Expression of drug targets remained largely unaffected by HDACi and AZA treatment. Importantly, cell viability, apoptosis, cell cycle dynamics and DNA damage were only affected by HDACi and/or AZA in ESCC and EAC, but not the non-neoplastic cells. This was specifically seen for the combination of MS-275 and AZA, leading to enhanced cancer cell selectivity and drug efficiency. By transcriptome analyses of MS-275, AZA and MS-275/AZA treated cells, known (e.g. p21) as well as novel regulated genes significantly associated with the cellular effects post HDACi and/or AZA treatment in ESCC and EAC cells were identified. Finally, human EC tissue specimens frequently expressed the actionable drug targets HDAC1/2/3 and DNMT1. In summary, a combined HDACi (MS-275)/AZA treatment is cancer cell selective and efficient in vitro. Since the majority of ECs express the drug targets in situ, this paves the way for further investigations of HDACi/AZA treatment in esophageal cancer cells and their translation into a clinico-pathological setting. To elucidate the transcriptome response to HDAC inhibitors of normal esophageal cells and esophageal tumor cells, total RNA was isolated from non-neoplastic esophageal epithelial cells (Het1A cells) a well as from two esophageal tumor cell lines (OE21 and OE33), respectively. Cells were treated with either MS-275, Azacytidine (AZA) or in combination of both. DMSO treatment was used as control in each case. Total RNA was isolated from cells 24 h after treatment and experiments were performed in biological triplicates.
2015-04-29 | E-GEOD-57130 | biostudies-arrayexpress