E-GEOD-65335
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA273718
PROVIDER: E-GEOD-65335 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-65335-analysis-methods.tsv | Tabular | |||
| E-GEOD-65335-analytics.tsv | Tabular | |||
| E-GEOD-65335-analytics.tsv.undecorated | Tabular | |||
| E-GEOD-65335-analytics.tsv.undecorated.unrounded | Tabular | |||
| E-GEOD-65335-analytics.tsv.unrounded | Tabular |
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Project description:Genome-wide expression profiling of an in vitro model for studying esophageal epithelial differentiation
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Project description:Tobacco in its smoke and smokeless form are major risk factors for ESCC (esophageal squamous cell carcinoma). However, molecular alterations associated with smokeless tobacco exposure are poorly understood. In the Indian subcontinent, tobacco is predominantly consumed in chewing form. An understanding of molecular alterations associated with chewing tobacco exposure is vital for identifying molecular markers and potential targets. We developed an in-vitro cellular model by exposing non-transformed esophageal epithelial cells to chewing tobacco over eight month period. Chronic exposure to chewing tobacco led to increase in cell proliferation, invasive ability and anchorage independent growth indicating cell transformation. Molecular alterations associated with chewing tobacco exposure were characterized by carrying out exome sequencing and quantitative proteomic profiling of parental cells and chewing tobacco exposed cells. Quantitative proteomic analysis revealed that established cancer stem cell markers are elevated in tobacco treated cells. Decreased expression of enzymes associated with the glycolytic pathway and increased expression of a large number of mitochondrially localized proteins involved in the electron transport chain as well as enzymes of TCA cycle were also identified. Electron micrographs revealed increase in number and size of mitochondria. Based on these observations, we hypothesise that chronic treatment of esophageal epithelial cells with tobacco leads to a cancer stem cell-like phenotype. These cells also show characteristic OXPHOS phenotype which can be potentially targeted as a therapeutic strategy.
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Project description:The interplay between genetic and environmental factors during pregnancy can predispose to inflammatory diseases postnatally, including eosinophilic esophagitis (EoE), a chronic allergic disease triggered by food. Herein, we examined the effects of amniotic fluid (AF) on esophageal epithelial differentiation and responsiveness to proallergic stimuli. Multiplex analysis of AF revealed the expression of 66 cytokines, whereas five cytokines including IL-4 and thymic stromal lymphopoietin (TSLP) were not detected. Several proinflammatory cytokines including TNFα and IL-12 were highly expressed in the AF from women who underwent preterm birth, whereas EGF was the highest in term birth samples. Exposure of esophageal epithelial cells to AF resulted in transient phosphorylation of ERK1/2 and the transcription of early response genes, highlighting the direct impact of AF on esophageal epithelial cells. In a three-dimensional spheroid model, AF modified the esophageal epithelial differentiation program and enhanced the transcription of IL-13-target genes, including CCL26 and CAPN14, which encodes for a major genetic susceptibility locus for eosinophilic esophagitis. Notably, CAPN14 exhibited upregulation in spheroids exposed to preterm but not term AF following differentiation. Collectively, our findings call attention to the role of AF as a potential mediator of the intrauterine environment that influences subsequent esophageal disorders.
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Project description:Despite advances and innovations in characterization of adult esophageal epithelial stem cells, there is still a gap in reliable in vitro methods that closely recapitulate human cell behavior in a physiological-in vivo relevant fashion. Therefore, in this data set we set up to bench mark a detailed single-cell atlas of adult human esophagus with matched in vitro model for long term culture.
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Project description:Eosinophilic esophagitis (EoE) is a chronic, allergic inflammatory disease of the esophageal mucosa. While type 2 cytokines are predominant, targeting type 2 inflammation alone is not always effective for all patients. In EoE patients, the transcriptional profiling of esophageal biopsy reveal upregulation of type I and II interferon (IFN) response, dysregulated immune signaling and downregulation of esophageal-specific genes in EoE patients. However, the role of interferon signaling during EoE is not fully understood. This study aims to investigate the impact of IFN signaling on esophageal epithelium and elucidate its role in EoE. IFN-γ stimulation of esophageal epithelial cells triggered disruption of tissue differentiation, epithelial barrier integrity and cytotoxicity, which are relevant features of EoE immunopathology. Beyond EoE, our findings offer insights into esophageal disorders which may involve increased IFN-γ signaling, including infections, gastrophageal reflux disease, and Barrett's esophagus.
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