HDAC-42 modulates acid-induced gene expression in human SEG-1 esophageal adenocarcinoma cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE7964 | GEO | 2007/07/30
SECONDARY ACCESSION(S): PRJNA100715
REPOSITORIES: GEO
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Project description:The role of acid and bile salts in the pathogenesis of esophageal carcinoma arising from Barrett's metaplasia has been well established. Cell proliferation of Barrett's epithelium in response to pulsatile acid exposure has since been confirmed in vivo using endoscopy specimens. Histone deactylases (HDACs) modulate nucleosomal packaging of DNA, thereby influencing gene transcription and multiple cancer-associated processes. Thus, we conducted microarray analysis to assess the ability of HDAC-42 to modulate key acid-induced changes as well as to impact other genes altered as the normal esophageal epithelium progresses along the metaplasia-dysplasia-esophageal adenocarcinoma continuum. Experiment Overall Design: SEG-1 cells were pretreated for 24 hours with vehicle or HDAC-42, pulsed with media or acidified media (pH 3.5; 20 mins at 37C), replenished with media or HDAC-42, and harvested 6 hours later. Global gene expression analysis was conducted using the human genome chip U133 2.0 Plus.
2008-06-15 | E-GEOD-7964 | biostudies-arrayexpress
Project description:To test the hypothesis that there is a specific miRNA expression signature which characterizes Barrett's esophagus development and progression, we performed miRNA microarray analysis comparing normal esophageal squamous epithelium with the two different metaplastic lesions occuring within Barrett's mucosa (i.e. gastric metaplasia and intestinal metaplasia). Samples of H. pylori-related gastritis and gastric intestinal metaplasia were also considered in the definition of esophageal-specific miRNAs. miRNA microarray analysis was performed in a series of samples obtained from (a) 10 histologically-proven long-segment Barrett's esophagus patients; (b) 10 patients with H. pylori-related chronic atrophic gastritis. Overall, 10 normal esophageal squamous epithelium samples, 10 esophageal intestinal metaplasia samples, 10 esophageal gastric metaplasia samples, 10 H. pylori -related gastritis samples (no atrophic lesion detected; obtained from the antrum) and 10 gastric intestinal metaplasia samples (obtained from the antrum) were considered.
2011-01-01 | E-GEOD-24839 | biostudies-arrayexpress
Project description:To test the hypothesis that there is a specific miRNA expression signature which characterizes Barrett's esophagus development and progression, we performed miRNA microarray analysis comparing normal esophageal squamous epithelium with the two different metaplastic lesions occuring within Barrett's mucosa (i.e. gastric metaplasia and intestinal metaplasia). Samples of H. pylori-related gastritis and gastric intestinal metaplasia were also considered in the definition of esophageal-specific miRNAs.
2011-01-01 | GSE24839 | GEO
Project description:Title: In vitro and in vivo effects of the orally bioavailable phenylbutyrate-derived histone deacetylase inhibitor OSU-HDAC42 on gene expression in esophageal tissues and in esophageal adenocarcinoma cells Histone deacetylases (HDACs) modulate nucleosomal packaging of DNA, thereby influencing gene transcription and multiple cancer-associated processes. Thus, we conducted microarray analysis at multiple time-points to assess the ability of OSU-HDAC42, the S enantiomer of the previously published compound HDAC-42, to modulate key acid-induced changes as well as to impact other genes altered as the normal esophageal epithelium progresses along the metaplasia-dysplasia-esophageal adenocarcinoma continuum. Keywords: acid-pulsed cells pretreated with OSU-HDAC42 or vehicle
2008-03-20 | GSE9974 | GEO
Project description:Barrett's esophagus is characterized by the replacement of squamous epithelium with specialized intestinal metaplastic mucosa. The exact mechanisms of initiation and development of Barrett's metaplasia remain unknown, but a hypothesis of successful adaptation against noxious reflux components has been proposed. To search for the repertoire of adaptation mechanisms of Barrett's metaplasia, we employed high-throughput functional genomic and proteomic methods that defined the molecular background of metaplastic mucosa resistance to reflux. Transcriptional profiling was established for 23 pairs of esophageal squamous epithelium and Barrett's metaplasia tissue samples using Affymetrix U133A 2.0 GeneChips and validated by quantitative real-time polymerase chain reaction. Differences in protein composition were assessed by electrophoretic and mass-spectrometry-based methods. Among 2,822 genes differentially expressed between Barrett's metaplasia and squamous epithelium, we observed significantly overexpressed metaplastic mucosa genes that encode cytokines and growth factors, constituents of extracellular matrix, basement membrane and tight junctions, and proteins involved in prostaglandin and phosphoinositol metabolism, nitric oxide production, and bioenergetics. Their expression likely reflects defense and repair responses of metaplastic mucosa, whereas overexpression of genes encoding heat shock proteins and several protein kinases in squamous epithelium may reflect lower resistance of normal esophageal epithelium than Barrett's metaplasia to reflux components. Despite the methodological and interpretative difficulties in data analyses discussed in this paper, our studies confirm that Barrett's metaplasia may be regarded as a specific microevolution allowing for accumulation of mucosal morphological and physiological changes that better protect against reflux injury. Department of Gastroenterology, Medical Center for Postgraduate Education and Maria SkM-EM-^Bodowska-Curie Memorial Cancer Center and Institute of Oncology, 02-781 Warsaw, Poland 2 types of tissue sample derived from the same patient: > Normal squamous epithelium (NE) from patients with longsegment of BarretM-bM-^@M-^Ys epithelium > Metaplastic epithelium from BarrettM-bM-^@M-^Ys esophagus (BE)
2012-03-08 | E-GEOD-36223 | biostudies-arrayexpress
Project description:Barrett's esophagus is characterized by the replacement of squamous epithelium with specialized intestinal metaplastic mucosa. The exact mechanisms of initiation and development of Barrett's metaplasia remain unknown, but a hypothesis of successful adaptation against noxious reflux components has been proposed. To search for the repertoire of adaptation mechanisms of Barrett's metaplasia, we employed high-throughput functional genomic and proteomic methods that defined the molecular background of metaplastic mucosa resistance to reflux. Transcriptional profiling was established for 23 pairs of esophageal squamous epithelium and Barrett's metaplasia tissue samples using Affymetrix U133A 2.0 GeneChips and validated by quantitative real-time polymerase chain reaction. Differences in protein composition were assessed by electrophoretic and mass-spectrometry-based methods. Among 2,822 genes differentially expressed between Barrett's metaplasia and squamous epithelium, we observed significantly overexpressed metaplastic mucosa genes that encode cytokines and growth factors, constituents of extracellular matrix, basement membrane and tight junctions, and proteins involved in prostaglandin and phosphoinositol metabolism, nitric oxide production, and bioenergetics. Their expression likely reflects defense and repair responses of metaplastic mucosa, whereas overexpression of genes encoding heat shock proteins and several protein kinases in squamous epithelium may reflect lower resistance of normal esophageal epithelium than Barrett's metaplasia to reflux components. Despite the methodological and interpretative difficulties in data analyses discussed in this paper, our studies confirm that Barrett's metaplasia may be regarded as a specific microevolution allowing for accumulation of mucosal morphological and physiological changes that better protect against reflux injury. Department of Gastroenterology, Medical Center for Postgraduate Education and Maria Skłodowska-Curie Memorial Cancer Center and Institute of Oncology, 02-781 Warsaw, Poland
2012-03-08 | GSE36223 | GEO
Project description:Title: In vitro and in vivo effects of the orally bioavailable phenylbutyrate-derived histone deacetylase inhibitor OSU-HDAC42 on gene expression in esophageal tissues and in esophageal adenocarcinoma cells; Histone deacetylases (HDACs) modulate nucleosomal packaging of DNA, thereby influencing gene transcription and multiple cancer-associated processes. Thus, we conducted microarray analysis at multiple time-points to assess the ability of OSU-HDAC42, the S enantiomer of the previously published compound HDAC-42, to modulate key acid-induced changes as well as to impact other genes altered as the normal esophageal epithelium progresses along the metaplasia-dysplasia-esophageal adenocarcinoma continuum. Experiment Overall Design: SEG-1 cells were pretreated for 24 hours with vehicle or OSU-HDAC42, pulsed with acidified media (pH 3.5; 20 mins at 37C), replenished with media or OSU-HDAC42, and harvested 3, 6 and 24 hours later. Global gene expression analysis was conducted using the human genome chip U133 2.0 Plus.
2008-04-05 | E-GEOD-9974 | biostudies-arrayexpress
Project description:Patients were recruited at the Departments of Abdominal Surgery and Endoscopy of the Hospital do Cancer AC Camargo (São Paulo/Brazil) during a 4-year period (2001 to 2004). All patients signed a pre-informed consent and the study was approved by the internal ethics committee. Tissue samples were either snap frozen in liquid nitrogen (when obtained by surgery) or collected in RNAlaterTM (Ambion®, Austin, Texas USA, when obtained by biopsy). For all samples, diagnosis was confirmed by H&E staining at the time of RNA extraction. Biopsy samples of the esophageal and gastric mucosa obtained by endoscopy had information of the correct anatomical location using a standard diagram. Frozen samples were dissected and only those having at least 70% of tumor cells were processed. A total of 71 samples were analyzed: 39 esophagus and esophagogastric junction samples (9 normal mucosa, 6 esophagitis mucosa, 10 Barrett's mucosa - 4 for the long type and 6 for the short type, and 14 tumor samples of adenocarcinoma) and 32 stomach samples (6 normal body and antrum mucosa, 5 normal cardiac mucosa, 9 intestinal metaplasia mucosa, 7 samples of intestinal type adenocarcinoma and 5 samples of diffuse type carcinoma). For Barrett's samples, diagnosis required evidence of intestinal metaplasia together with tongues or segments of red columnar-appearing epithelium extending upwards from the esophagogastric junction. A long Barrett's esophagus was defined as longer ?3cm and a short Barrett's esophagus by ?3cm of columnar epithelium (Spechler, 2004). The tumor samples of esophagus and esophagogastric junction were not differentiated. For the gastric adenocarcinoma samples were used the Laurén's classification (Laurén, 1965) and the others gastric sample were previously described (Meireles et al, 2003). Keywords: other
2005-05-09 | GSE2444 | GEO
Project description:To test the hypothesis that there is a specific miRNA expression signature which characterizes Barrett's esophagus development and progression, we performed miRNA microarray analysis comparing normal esophageal squamous epithelium with all the phenotypic lesions seen in the Barrett's carcinogenic process miRNA microarray analysis was performed in a series of 14 normal esophageal squamous epithelium samples, 14 Barrett's mucosa samples, 7 low-grade intra-epithelial neoplasia samples, 5 high-grade intra-epithelial neoplasia samples and 11 Barrett's adenocarcinoma samples
2010-01-29 | E-GEOD-20099 | biostudies-arrayexpress
Project description:Cdx2 has been suggested to play an important role in Barrett's esophagus (BE), or intestinal metaplasia (IM) in the esophagus. However, in vivo data have been lacking. The aim of the present study was to investigate whether transgenic overexpression of zCdx1b, the functional equivalent of mammalian Cdx2 in zebrafish, may lead to IM of squamous epithelium in zebrafish A transgenic zebrafish system was developed by expressing zCdx1b gene under the control of zebrafish keratin 5 promoter (zK5p). zCdx1b expression in the esophageal squamous epithelium of transgenic zebrafish was analyzed by in situ hybridization, immunohistochemical staining and RT-PCR. Gene expression in the esophageal squamous epithelium of wild-type and transgenic zebrafish was analyzed by Affymetrix microarray and confirmed by in situ hybridization.
2012-02-18 | GSE35889 | GEO