E-GEOD-42937
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA183893
PROVIDER: E-GEOD-42937 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-42937-analysis-methods.tsv | Tabular | |||
| E-GEOD-42937-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-42937-configuration.xml | Xml | |||
| E-GEOD-42937-percentile-ranks.tsv | Tabular | |||
| E-GEOD-42937.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 90 |
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Project description:Gastric cancer is still one of the most common causes of cancer-related death worldwide, which is mainly attributable to late diagnosis and poor treatment options. Infection with H. pylori, different environmental factors and genetic alterations are known to influence the risk of developing gastric tumors. However, the molecular mechanisms involved in gastric carcinogenesis are still not fully understood, making it difficult to design targeted therapeutic approaches. Aberrant expression of the specific gastric differentiation marker Sox2 (sry-related HMG box 2) has been observed in stomach cancer. However, the role of Sox2 in gastric tumors has not been well established to date. To elucidate the role of Sox2 in gastric tumorigenesis, Sox2 transcriptional activity was blocked in AZ521 cells. Interestingly, inhibition of Sox2 reduced cell proliferation and migration, increased apoptosis and induced changes in cell cycle. Blocking of Sox2 also reduced the tumorigenic potential of AZ521 cells in vivo. In addition, correlation of Sox2 expression and proliferation was observed in a subset of human gastric tumours. Finally, target genes of Sox2 were for the first time identified by RNA microarray in gastric cancer cells. Taken together, the results presented here indicate that Sox2 controls several aspects related to gastric cancer development and progression by regulating the expression of members of important signalling pathways. These findings could provide new therapeutic options for a subset of gastric cancers exhibiting Sox2 deregulation. Inducible dnSox2 in AZ521 cells, 4 timepoints with/without induction.
2013-12-31 | E-GEOD-42937 | biostudies-arrayexpress
Project description:Doxycycline, a tetracycline based antibiotic which has bacteriostatic activity against a broad range of both gram positive and gram negative bacteria was identified to inhibit the expression of ERK/MAPK signaling pathway in gastric cancer. ERK/MAPK pathway is one of the highly activated and a crucial player in gastric cancer progression. To delineate the complex transcription program associated with ERK/MAPK pathway and thus inhibited by doxycycline in gastric cancer cells, doxycycline was treated in AGS, one of the ERK/MAPK overexpressed gastric cancer cell line. The resulatant changes in genome-wide mRNA expression pattern between control and doxycycline treated was profiled using Human Transcriptome 2.0 arrays.
2021-01-06 | GSE124022 | GEO
Project description:Gastric cancer is still one of the most common causes of cancer-related death worldwide, which is mainly attributable to late diagnosis and poor treatment options. Infection with H. pylori, different environmental factors and genetic alterations are known to influence the risk of developing gastric tumors. However, the molecular mechanisms involved in gastric carcinogenesis are still not fully understood, making it difficult to design targeted therapeutic approaches. Aberrant expression of the specific gastric differentiation marker Sox2 (sry-related HMG box 2) has been observed in stomach cancer. However, the role of Sox2 in gastric tumors has not been well established to date. To elucidate the role of Sox2 in gastric tumorigenesis, Sox2 transcriptional activity was blocked in AZ521 cells. Interestingly, inhibition of Sox2 reduced cell proliferation and migration, increased apoptosis and induced changes in cell cycle. Blocking of Sox2 also reduced the tumorigenic potential of AZ521 cells in vivo. In addition, correlation of Sox2 expression and proliferation was observed in a subset of human gastric tumours. Finally, target genes of Sox2 were for the first time identified by RNA microarray in gastric cancer cells. Taken together, the results presented here indicate that Sox2 controls several aspects related to gastric cancer development and progression by regulating the expression of members of important signalling pathways. These findings could provide new therapeutic options for a subset of gastric cancers exhibiting Sox2 deregulation.
2013-12-31 | GSE42937 | GEO
Project description:The transcription factor Sox2 inhibits human gastric cancer growth and activates Sox2-related tumor surpressive genes in human gastric cancer cells. Conditional Sox2-overexpression in cells with a low Sox2 level demonstrated that the Sox2-regulated tumor surpressive genes demand on an enhanced Sox2 activity for better expression to work in human gastric cancer. Chromatin immunoprecipitation (ChIP) of Sox2 together with chromatin profiling by ChIP-on-chip analysis demonstrated that Sox2 directly activates the chromatin at promoters or putative enhancers of Sox2 target genes. Transcription factor Sox2 promoter array in MKN28 cells with Sox2 overexpression.
2013-05-22 | E-GEOD-45427 | biostudies-arrayexpress
Project description:The transcription factor Sox2 inhibits human gastric cancer growth and activates Sox2-related tumor surpressive genes in human gastric cancer cells. Conditional Sox2-overexpression in cells with a low Sox2 level demonstrated that the Sox2-regulated tumor surpressive genes demand on an enhanced Sox2 activity for better expression to work in human gastric cancer. Chromatin immunoprecipitation (ChIP) of Sox2 together with chromatin profiling by ChIP-on-chip analysis demonstrated that Sox2 directly activates the chromatin at promoters or putative enhancers of Sox2 target genes.
2013-05-22 | GSE45427 | GEO
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
Project description:To assess cellular changes upon abrogation of the WNT-signaling pathway, we induced expression of a dominant-negative T-cell factor 4 (TCF4). This showed a remarkable overlap with activation of the unfolded protein response (UTR) in the same colon cancer cell line. 500,000 cells were plated in a 10 cm2 plate, and the following day, treated for 20 hrs with doxycycline (Dox) or vehicle. Three independent biological replicates per treatment.
2015-04-01 | E-GEOD-28467 | biostudies-arrayexpress
Project description:Purpose: Sox2 expression marks gastric stem and progenitor cells, raising important questions regarding the genes regulated by Sox2 and the role of Sox2 itself during stomach homeostasis and disease. The goal of this study is to determine the function of and the genes regulated by Sox2 in the stomach. Methods: Sox2 ChIP-enriched DNA and input DNA was isolated from gastric glands of adult antrum from Sox2 KO and Sox2 WT mice. DNA was purified and genomic libraries were prepared as described (Sulahian et al., 2014), using four micrograms of goat anti-SOX2 (AF2018, R&D). Libraries were sequenced (50 bp, single-end reads) on an Illumina Hi-Seq 2000 instrument. Results: Sox2 is dispensiable for gastric stem cell self-renewal and epithelial homeostasis, however modulates the expression of wnt, intestinal and cancer related genes Examination of Sox2 targets in the stomachs of Sox2 WT and Sox2 KO mice.
2016-08-04 | E-GEOD-83965 | biostudies-arrayexpress
Project description:To identify candidate downstream target genes of SOX2 in gastric cancer cells, we transiently expressed exogenous SOX2 in a gastric cancer cell line NUGC3 and analyzed significant changes of gene expression.
2011-02-02 | GSE23589 | GEO
Project description:Purpose: Sox2 expression marks gastric stem and progenitor cells, raising important questions regarding the genes regulated by Sox2 and the role of Sox2 itself during stomach homeostasis and disease. The goal of this study is to determine the function of and the genes regulated by Sox2 in the stomach. Methods: Sox2 ChIP-enriched DNA and input DNA was isolated from gastric glands of adult antrum from Sox2 KO and Sox2 WT mice. DNA was purified and genomic libraries were prepared as described (Sulahian et al., 2014), using four micrograms of goat anti-SOX2 (AF2018, R&D). Libraries were sequenced (50 bp, single-end reads) on an Illumina Hi-Seq 2000 instrument. Results: Sox2 is dispensiable for gastric stem cell self-renewal and epithelial homeostasis, however modulates the expression of wnt, intestinal and cancer related genes
2016-08-04 | GSE83965 | GEO