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Expression data from cultured human esophageal squamous cell carcinoma cell lines and cultured human fibroblasts.

ABSTRACT: Cancer cells express different sets of receptor type tyrosine kinases. These receptor kinases may be activated through autocrine or paracrine mechanisms. Fibroblasts may modify the biologic properties of surrounding cancer cells through paracrine mechansms. We used microarrays to obtain the global gene expression of human esophageal squamous cell carcinoma cell lines and various esophageal fibroblasts.

ORGANISM(S): Homo sapiens

PROVIDER: GSE63941 | GEO | 2014/12/09

SECONDARY ACCESSION(S): PRJNA269575

REPOSITORIES: GEO

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Expression data from cultured human esophageal squamous cell carcinoma cell lines and cultured human fibroblasts.

Project description:Cancer cells express different sets of receptor type tyrosine kinases. These receptor kinases may be activated through autocrine or paracrine mechanisms. Fibroblasts may modify the biologic properties of surrounding cancer cells through paracrine mechansms. We used microarrays to obtain the global gene expression of human esophageal squamous cell carcinoma cell lines and various esophageal fibroblasts. A total of 22 human esophageal squamous cell carcinoma cell lines and fibroblasts were analyzed. 4 fibroblasts were obtained from surgically resected human esophagus. Cells were cultured under standard conditions, total RNA was extracted and hybridized on Affymetrix microarrays.

2014-12-09 | E-GEOD-63941 | biostudies-arrayexpress

Effects of IL-13 on primary esophageal fibroblasts

Project description:This is part of a larger experiment in which the effects of IL-13, LIGHT and TGF-B1 on human primary esophageal fibroblasts were analyzed and compared.

2022-09-29 | GSE212731 | GEO

Esophageal keratinocyte invasion after loss of E-cadherin and TGF receptor type II

Project description:Esophageal cancer is one of the deadliest cancers as patients present at late stages of disease. Frequent gene alterations include the loss of E-cadherin and TGFb receptor type II. The goal of this study was to establish a model of esophageal cancer by introducing dominant-negative mutants of E-cadherin and TGFb receptor II. To analyze the functional consequences and gene expression chages induced by E-cadherin and TGFb receptor type II loss in esophageal cancer. Human esophageal keratinocytes were retrovirally transfected with wild-type full length E-cadherin, dominant-negative E-cadherin and dominant-negative TGFb receptor type II. Grown in organotypic cultures on a collagen/matrigel matrix with embedded fibroblast, the generated cell lines were analyzed for their potential to invade into the underlying matrix. Each cell lines was grown in duplicate in organotypic culture and therefore 2 replicates analyzed. Gene expression changes in invasive versus non-invasive areas were analyzed after RNA isolation using laser-capture microdissection resulting in 2 samples representing a normal esophageal epithelium (Ecad), 2 each of dominant-negative Ecad (Ecyto) non-invasive and invasive. To model the genetic alterations in esophageal cancer dominant-negative E-cadherin and dominant-negative TGFb receptor type II (Ecyto-dnTGFR) were expressed and 2 samples each, non-invasive and invasive, analyzed.

2013-11-12 | E-GEOD-19472 | biostudies-arrayexpress

Comparison of the LIGHT and TGF-B1 induced transcriptomes in esophageal FBL

Project description:To understand the transcriptional responses induced by LIGHT in esophageal fibroblasts and compare them to the pro-fibrotic TGF-B1

2020-08-03 | GSE143482 | GEO

Esophageal keratinocyte invasion after loss of E-cadherin and TGF receptor type II

2013-11-12 | GSE19472 | GEO

Transcriptomes Analysis of 4NQO induced-esophageal tumors of Wild Type and S100A14 CKO mice

Project description:Purpose: To fully realize the potential molecular mechanism that S100A14 deficiency enhances esophageal carcinogenesis Methods: Total RNA of esophageal tumors in 4NQO WT and 4NQO S100A 14 CKO group mice was extracted with TRIzol Reagent. RNA libraries were constructed using an Illumina TruSeq RNA Sample Preparation kit according to the manufacturer’s protocol. A total of 150 base paired-end reads were sequenced using the Novaseq 6000 S4 platform. The read alignment was conducted using TopHat 2.0.13, and relative transcript abundances and differentially expressed genes were determined using the DESeq R package. Results: We identified 14,157 transcripts in esophageal tumors of 4NQO WT and 4NQO S100A14 CKO group mice. Approximately 8% of the transcripts showed differential expression between the esophageal tumors of 4NQO WT and 4NQO S100A 14 CKO group mice, with a fold change ≥1.0 and p value <0.05. Conclusions: Our study represents the first analysis of esophageal tumors derived from S100A14 CKO mice with biologic replicates, generated by RNA-seq.

2022-07-07 | GSE200772 | GEO

Esophageal Adenocarcinoma

Project description:Esophageal Adenocarcinoma

| PRJNA188928 | ENA

Barrett's esophageal tissues and esophageal adenocarcinoma specimens

Project description:This SuperSeries is composed of the following subset Series: GSE37200: Gene expression profiling of Barrett’s esophageal tissues and esophageal adenocarcinoma specimens GSE37201: Gene expression profiling of esophageal adenocarcinoma Refer to individual Series

2012-04-10 | E-GEOD-37203 | biostudies-arrayexpress

Lipidomics of esophageal adenocarcinoma

Project description:Lipidomics of esophageal adenocarcinoma

2021-08-22 | ST001942 | MetabolomicsWorkbench

Expression data from glioblastoma stem-like cells (GSCs) and astrocyte co-cultured GSCs

Project description:consequences of astrocytes on GSCs, gene expression profiles generated from glioblastoma stem-like cells grown alone (mono-culture) and compared to those generated 48h after the initiation of co-culture with astrocytes We used microarrays show that astrocytes are capable to modify via a paracrine mechanism GSC gene expression and thus phenotype.

2014-11-07 | GSE63037 | GEO

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