Genomic and transcriptomic profiles of the gastric cancer-prone environment
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PROVIDER: PRJEB47259 | ENA |
REPOSITORIES: ENA
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Project description:Helicobacter pylori colonization of the human stomach is a strong risk factor for gastric cancer. To investigate H. pylori-induced gastric molecular alterations, we used a Mongolian gerbil model of gastric carcinogenesis. Histologic evaluation revealed varying levels of atrophic gastritis (a premalignant condition characterized by parietal and chief cell loss) in H. pylori-infected animals, and transcriptional profiling revealed a loss of markers for these cell types. We then assessed the spatial distribution and relative abundance of proteins in the gastric tissues using imaging mass spectrometry and liquid chromatography with tandem mass spectrometry (LC-MS/MS). We detected striking differences in protein content of corpus and antrum tissues. 492 proteins were preferentially localized to the corpus in uninfected animals. The abundance of 91 of these proteins was reduced in H. pylori-infected corpus tissues exhibiting atrophic gastritis compared to infected corpus tissues with non-atrophic gastritis or uninfected corpus tissues; these included numerous proteins with metabolic functions. Fifty proteins localized to the corpus in uninfected animals were diffusely delocalized throughout the stomach in infected tissues with atrophic gastritis; these included numerous proteins with roles in protein processing. Corresponding alterations were not detected in animals infected with a H. pylori ∆cagT mutant (lacking Cag type IV secretion system activity). These results indicate that H. pylori can cause loss of proteins normally localized to the gastric corpus as well as diffuse delocalization of corpus-specific proteins, resulting in marked changes in the normal gastric molecular partitioning into distinct corpus and antrum regions.
2023-12-04 | PXD046333 | Pride
Project description:Regions of recurrent genomic amplification and deletion are frequently observed in primary gastric cancers (GC). However, identifying specific oncogenes and tumor suppressor genes within these regions can be challenging, as they often cover tens to hundreds of genes. Here, we combined high-resolution array-based comparative genomic hybridization (aCGH) with gene expression profiling to target genes lying within focal high-level amplifications in GC cell lines, and identified RAB23 as an amplified and overexpressed Chr 6p11p12 gene in Hs746T cells. High RAB23 protein expression was also observed in some lines lacking RAB23 amplification, suggesting additional mechanisms besides gene amplification for up-regulating RAB23. siRNA silencing of RAB23 reduced the invasive potential of both amplified and nonamplified GC cell lines. RAB23 gene amplifications were observed in 13% of primary gastric carcinomas. In two independent patient cohorts, RAB23 transcript and protein expression was significantly associated with diffuse-type gastric cancer (dGC) compared to intestinal-type gastric cancer (iGC), providing further evidence that dGC and iGC likely represent two molecularly distinct tumor types. Our study demonstrates that investigating focal chromosomal amplifications by combining highresolution aCGH with expression profiling is a powerful general strategy for identifying novel cancer genes in recurrent regions of chromosomal aberration. Keywords: gastric cancer cell lines, comparative genomic hybridization, gene expression profiling Affy 100K SNP profiling and 32K BAC Array profiling for 7 Gastric Cancer Cell Lines
2010-05-14 | E-GEOD-10611 | biostudies-arrayexpress
Project description:Sequencing of 16S ribosomal RNA (rRNA) gene, which has improved the characterization of microbial community, has made it possible to detect a low level Helicobacter pylori (HP) sequences even in HP-negative subjects which were determined by a combination of conventional methods. This study was conducted to obtain a cutoff value for HP colonization in gastric mucosa biopsies and gastric juices by the pyrosequencing method. Corresponding author: Department of Internal Medicine, Seoul National University Bundang Hospital, Seoungnam, Gyeonggi-do, Korea; Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul, Korea (Tel., +82-31-787-7008; e-mail, nayoungkim49@empas.com). Microbial DNA from gastric mucosal samples [gastric antrum (n=63, mucosal biopsy), follow-up sample on gastric antrum (n=16, mucosal biopsy), and gastric body (n=18, mucosal biopsy)] and gastric juices (n=4, not mucosal biopsy) was amplified by nested PCR using universal bacterial primers, and the 16S rRNA genes were pyrosequenced.
2014-09-18 | E-GEOD-61493 | biostudies-arrayexpress
Project description:Copy number profiling of 27 gastric cancer cell lines and 105 gastric tumor tissues. we hypothesized that a detailed fine-scale survey of genomic CNAs might reveal potential genes disrupted by fusion events in gastric cancer. We inferred the locations of likely chromosomal breakpoints by identifying regions where closely-spaced microarray probes exhibited striking transitions in copy number. 27 gastric cancer cell lines and 105 gastric tumor tissues were profiled by Agilent 244K microarray.
2010-12-31 | E-GEOD-22694 | biostudies-arrayexpress
Project description:Regions of recurrent genomic amplification and deletion are frequently observed in primary gastric cancers (GC). However, identifying specific oncogenes and tumor suppressor genes within these regions can be challenging, as they often cover tens to hundreds of genes. Here, we combined high-resolution array-based comparative genomic hybridization (aCGH) with gene expression profiling to target genes lying within focal high-level amplifications in GC cell lines, and identified RAB23 as an amplified and overexpressed Chr 6p11p12 gene in Hs746T cells. High RAB23 protein expression was also observed in some lines lacking RAB23 amplification, suggesting additional mechanisms besides gene amplification for up-regulating RAB23. siRNA silencing of RAB23 reduced the invasive potential of both amplified and nonamplified GC cell lines. RAB23 gene amplifications were observed in 13% of primary gastric carcinomas. In two independent patient cohorts, RAB23 transcript and protein expression was significantly associated with diffuse-type gastric cancer (dGC) compared to intestinal-type gastric cancer (iGC), providing further evidence that dGC and iGC likely represent two molecularly distinct tumor types. Our study demonstrates that investigating focal chromosomal amplifications by combining highresolution aCGH with expression profiling is a powerful general strategy for identifying novel cancer genes in recurrent regions of chromosomal aberration. Keywords: gastric cancer cell lines, comparative genomic hybridization, gene expression profiling
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Project description:Human gastric mucosal samples Metagenome
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Project description:Helicobacter pylori (H. pylori) infection is associated with an inflammatory response in the gastric mucosa, ultimately leading to cellular hyperproliferation and malignant transformation. Hitherto, only expression of a single gene, or a limited number of genes, has been investigated in infected patients. Thus, the impact of H. pylori on the expression of a broad set of genes has not yet been analyzed. cDNA arrays were therefore used to establish the global pattern of gene expression in gastric tissue of healthy subjects and of H. pylori infected patients. Two main gene expression profiles were identified based on cluster analysis. The data obtained suggest a strong involvement of selected Toll-like receptors (TLRs)3, adhesion molecules, chemokines, and interleukins in the mucosal response. This pattern is clearly different from that observed using gastric epithelial cell lines infected in vitro with H. pylori. The genotype of the bacteria (presence of genes encoding CagA, VacA and BabA) was analyzed by PCR and shown to be associated with different expression profiles. The presence of a Keywords = H. pylori Keywords = gastric inflammation Keywords = cytokines Keywords: parallel sample
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Project description:Copy number profiling of 27 gastric cancer cell lines and 105 gastric tumor tissues. we hypothesized that a detailed fine-scale survey of genomic CNAs might reveal potential genes disrupted by fusion events in gastric cancer. We inferred the locations of likely chromosomal breakpoints by identifying regions where closely-spaced microarray probes exhibited striking transitions in copy number.
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