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Homo sapiens

ABSTRACT: SOX15 governs a transcriptional program in human esophageal stratified epithelium and in a subset of esophageal adenocarcinomas

PROVIDER: PRJNA266111 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1804790.fastq.gz	Fastqsanger.gz
	SRR1804791.fastq.gz	Fastqsanger.gz
	SRR1804792.fastq.gz	Fastqsanger.gz
	SRR1804793.fastq.gz	Fastqsanger.gz
	SRR1804794.fastq.gz	Fastqsanger.gz

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SOX15 governs a transcriptional program in human esophageal stratified epithelium and in a subset of esophageal adenocarcinomas

2015-11-09 | GSE62909 | GEO

SOX15 governs a transcriptional program in human esophageal stratified epithelium and in a subset of esophageal adenocarcinomas

Project description:We identified spatially restricted transcription factors and found SOX15 expression confined to stratified esophageal epithelium, with attenuation in Barrett's esophagus. SOX15 binds esophagus-specific loci and its loss in human esophageal cells affected esophagus-specific transcripts [RNA-Seq] Total RNA isolated from CPA control cells and CPA cells following SOX15 depletion, samples were prepared for sequencing using the TruSeq RNA Sample Preparation Kit (Illumina) according to the manufacturer's instructions. 75 base pair single-end reads were sequenced on an Illumina NextSeq 500 instrument. The data include 2 independent biological replicates per genotype. [ChIP-Seq] Examine SOX15-chromatin binding in CPA cells.

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Project description:We established an efficient protocol to generate esophageal epithelial progenitors (EPCs) from human pluripotent stem cells (hPSCs). Inhibition of TGFß and BMP signaling is required for the differentiation of hPSCs into EPCs which can be further purified with EPCAM and Integrin ß4. These purified EPCs express human fetal esophageal genes and recapitulate the normal development of the stratified squamous epithelium. We performed global transcriptomic profiling of E12.5 mouse embryonic esophageal epithelia, human fetal esophageal epithelia and human embryonic stem cell RUES2-derived esophageal progenitor cells through RNA sequencing. We found that these cells shared similar expression of NOTCH components including Jag1 and 2, Dll1, 3 and 4, and Notct1, 3, 4. The gene expression profile allows to understand transcriptional program in mouse and human developing esophagus.

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Project description:Human esophageal adenocarcinomas

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Project description:Samples were obtained from 8 patients with Barrett's associated adenocarcinomas after transhiatal esophagectomy. Samples representative of the normal esophageal epithelium (N), BarrettÃ¢ÂÂs esophagus (B) and esophageal adenocarcinomas (ADC) were obtained from every patient by experienced GI pathologists. RNA were extracted and samples were profiled for detection of genes differentially expressed in B and ADC relative to N and in ADC relative to B.

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Barrett's esophagus, Barrett's-associated adenocarcinomas and normal esophageal epithelium

Project description:Samples were obtained from 8 patients with Barrett's associated adenocarcinomas after transhiatal esophagectomy. Samples representative of the normal esophageal epithelium (N), Barrett’s esophagus (B) and esophageal adenocarcinomas (ADC) were obtained from every patient by experienced GI pathologists. RNA were extracted and samples were profiled for detection of genes differentially expressed in B and ADC relative to N and in ADC relative to B. Keywords: other

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Generation of esophageal organoids from human pluripotent stem cells and their use to study human development

Project description:Tracheoesophageal disorders and diseases are prevalent in humans such that an organoid model of human esophagus could be greatly beneficial. We therefore established a three-dimensional esophageal organoid culture system through the directed differentiation of human pluripotent stem cells (hPSCs). We identified that sequential manipulation of several signaling pathways resulted in patterning of definitive endoderm to dorsal anterior foregut spheroids (dAFGs). Outgrowth of dAFGs for 1-2 months resulted in human esophageal organoids (HEOs) with a stratified squamous epithelium comparable to a late gestation mouse embryonic esophagus. These 1 and 2 month old HEOs were harvested for RNA to transcriptionally profile and compare them to profiles of esophageal tissue biopsies and keratinocytes. We then used HEOs and mouse embryos to identify how SOX2 mediates separation of the esophageal and respiratory lineages and found that loss of endodermal Sox2 results in complete esophageal agenesis. Using a SOX2 CRISPR interference iPS line, we generated dorsal and ventral anterior foregut progenitors (by manipulating BMP signaling) with or without SOX2-knockdown. At the transcriptional level, SOX2 acts to promote esophageal specification in both mice and humans in part by inhibiting Wnt signaling in the dorsal AFG and promoting survival of esophageal epithelium. In addition to this use of hPSC-derived esophageal organoids to study development, HEOs can be used for future studies of esophageal pathologies, such as Barrett’s metaplasia and carcinoma.

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Project description:The esophagus is protected from the hostile environment by a stratified epithelium, which renews rapidly. Homeostasis of this epithelium is ensured by a rare population of stem cells in the basal layer: Keratin 15+ (Krt15+) cells. However, little is known about the molecular mechanisms regulating their distinct features, namely self-renewal, potency, and epithelial regeneration. Achaete-Scute Family BHLH Transcription Factor 2 (ASCL2) is strongly upregulated in Krt15+ stem cells and is known to contribute to stem cell maintenance in other tissues. Herein, we investigated the role of ASCL2 in maintaining homeostasis under normal and stress conditions in the esophageal epithelium. ASCL2 overexpression severely dysregulated cell differentiation and cell fate. Proliferation was also reduced due potentially to a blockage in the G1 phase of the cell cycle or an induction of quiescence. Mass spectrometry analysis confirmed alterations in several proteins associated with differentiation and cell cycle. In addition, overexpression of ASCL2 enhanced resistance to radiation and chemotherapeutic drugs. Overall, these results denoted the role of ASCL2 as a key regulator of the proliferation-differentiation equilibrium in the esophageal epithelium.

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Homo sapiens

Project description:Barrett's esophagus, Barrett's-associated adenocarcinomas and normal esophageal epithelium

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