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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genes regulated by SET7/9 knockdown in gastric cancer cells

ABSTRACT: Expression of SET7/9, a histone methyltransferase, was frequently reduced in cultured and primary gastric cancers. To identify the SET7/9 target genes in gastric cancer, we performed siRNA-based knockdown of SET7/9 in MKN74 and MKN45 cells and then examined significant expression changes of genes by microarray. Transfection of SET7/9 siRNA into MKN74 and MKN45 cells were performed by electroporation. After 48hrs, cells were harvested. Total RNA was used for cDNA microarray.

ORGANISM(S): Homo sapiens

SUBMITTER: Yoshimitsu Akiyama

PROVIDER: E-GEOD-59834 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genes regulated by SET7/9 knockdown in gastric cancer cells

Project description:Expression of SET7/9, a histone methyltransferase, was frequently reduced in cultured and primary gastric cancers. To identify the SET7/9 target genes in gastric cancer, we performed siRNA-based knockdown of SET7/9 in MKN74 and MKN45 cells and then examined significant expression changes of genes by microarray.

2015-07-24 | GSE59834 | GEO

Oncogenic roles of SETDB2 histone methyltransferase in gastric cancer

Project description:Histone H3 lysine 9 tri-methyltransferases (H3K9me3) are related to transcriptional gene silencing. Although SETDB2 has H3K9me3 activity, it is unknown whether SETDB2 is linking to carcinogenesis. Here, we studied alterations and functions of SETDB2 in gastric cancers (GCs). In human clinical samples, overexpression of SETDB2 protein was observed in 30 of 72 (41.7%) primary GC tissues compared with their normal counterparts, and significantly associated with poor prognosis of the patients (P<0.05). SETDB2 protein was significantly detected in late stage of GCs. Moreover, SETDB2 protein was strongly expressed in four (30.8%) of 13 GC cell lines, and knockdown of SETDB2 led to decrease the cell proliferation, migration and invasion. According to the microarray analysis on a GC cell line after knockdown of SETDB2, the expression of WWOX and CADM1 tumor suppressor genes was significantly up-regulated. ChIP analysis showed that the H3K9me3 levels at the promoter regions of WWOX and CADM1 genes were closely regulated by the SETDB2 in GC cells. We also found that SETDB2 bound to the promoter regions after SETDB2 overexpression. Our data suggest that SETDB2 is associated with transcriptional repression of WWOX and CADM1, through H3K9me3, and hence overexpression of SETDB2 may contribute to gastric progression. Transfection of SETDB2 siRNA into MKN74 cells were performed by electroporation. After 48hrs, cells were harvested. Total RNA was used for cDNA microarray.

2016-02-21 | E-GEOD-76135 | biostudies-arrayexpress

MKN74 gastric epithelial cells infected with Enterococcus faecalis for 24hrs or 5day

Project description:MKN74 cells were infected for 24 h or 5 days. For the 24 h infection, 80% confluent MKN74 cells were washed three times in PBS and incubated in antibiotic free medium. Overnight-grown colonies of E. faecalis were collected and added to the MKN74 cell culture at a multiplicity of infection (MOI) of 50 bacteria per cell. Cultures were maintained at 37 C under a 5% CO2 humidified atmosphere. 5 day infections were carried out by treating 65% confluent MKN74 cells with E. faecalis at a MOI of 10. Every 24 h, cells were washed three times with PBS and fresh medium and bacteria were added. Control cells were processed similarly in the absence of bacteria.

2012-04-02 | E-MEXP-3496 | biostudies-arrayexpress

Changes in gene expression in MKN45 cells in response to Helicobacter pylori lipopolysaccharide

Project description:This study set out to identify global changes in gene expression in MKN45 gastric epithelial cells following 8 hours stimulation with 10 μg/ml lipopolysaccharide (LPS) from the gastric pathogen H. pylori. Microarray analysis was used to compare changes in gene expression between cells treated with 10 μg/ml H. pylori LPS and untreated cells at the same time point. Total RNA was harvested from MKN45 cells following treatment with LPS for 8h or untreated cells at the same time-point. 2 independent experiments were carried out. RNA was labeled and hybridized to GeneChips to analyse changes in gene expression.

2011-01-12 | E-GEOD-25147 | biostudies-arrayexpress

Gene expression signatures in miR-29c overexpressed gastric cancer cells.

Project description:To explain the mechanism that miR-29c affects the cell proliferation, we attempted to identify the miR-29c target genes in gastric carcinoma. The expression profiles in MKN45, MKN7 and MKN74 cells transfected with miR-29c oligo or Negative control oligo were obtained from microarray analysis. Then, the genes differentially expressed (Fold change >= 2.0) in miR-29c-transfected cells compared with negative control-transfected ones were identified in each cell lines, respectively. The differentially expressed genes shared among 3 cell lines were identified as the candidates for miR-29c targets. Human gastric cancer cell lines, MKN45, MKN74 and MKN7 were transfected with miR-29c oligo or negative control oligo (n=2) (Ambion). At 24h after, total RNA was extracted and microarray analysis was performed. The genes with common expression changes among three cell lines miR-29c-transfected were identified as the candidates for miR-29c targets.

2013-03-27 | E-GEOD-38581 | biostudies-arrayexpress

Human gastric cancer cell MKN45: MKN45-GFP control vs. highly metastatic sublines

Project description:Gene expression profiles of in vitro selected highly metastatic MKN45-GFP sublines. The results were compared with MKN45-GFP control cell line to determine the metastasis associated genes. Four pairs compared experiment. Each pair was used MKN45-GFP cells as correlated control. Determining on the gene expression trends were by various metastatic ability of each subline.

2011-11-10 | E-GEOD-33570 | biostudies-arrayexpress

Epigenetic silencing of miR-210 increases the proliferation of gastric epithelium during chronic Helicobacter pylori infection

Project description:Persistent colonization of the gastric mucosa by Helicobacter pylori (Hp) elicits chronic inflammation and aberrant epithelial cell proliferation, which increases the risk of gastric cancer. We examined the ability of microRNAs to modulate gastric cell proliferation in response to persistent Hp infection and found that epigenetic silencing of miR-210 plays a key role in gastric disease progression. Importantly, DNA methylation of the miR-210 gene was increased in Hp-positive human gastric biopsies as compared to Hp-negative controls. Moreover silencing of miR-210 in gastric epithelial cells promoted proliferation. We identified STMN1 and DIMT1 as miR-210 target genes and demonstrated that inhibition of miR-210 expression augmented cell proliferation by activating STMN1 and DIMT1. Together, our results highlight inflammation-induced epigenetic silencing of miR-210 as a mechanism of induction of chronic gastric diseases, including cancer, during Hp infection. To identify miR-210 targets in gastric cells, whole transcriptome analysis of AGS and MKN45 cells transfected with pre-miR-210 was conducted using Affymetrix GeneChip Human Genome U133 Plus 2.0 Array.

2014-09-04 | E-GEOD-58004 | biostudies-arrayexpress

MET Amplified Gastric Cancer Cell Lines +/- Crizotinib

Project description:MET amplification is present in 20% of gastric cancers and has been confirmed as a therapeutic target in clinical trials. The molecular mechanisms of response and resistance to MET inhibitors are not well understood. We investigated the determinants of MET dependency in human gastric cancer. MET inhibition inhibited proliferation and induced cell death only in MET-amplified gastric cancer cell lines. The effects on growth arrest were stronger than the effects on cell death. To identify possible resistance mechanisms, we performed whole-genome mRNA expression profiling. Molecular changes related to autophagy were among the top alterations observed. Consistent with these findings, autophagy levels increased in a concentration-dependent manner when MET-amplified cells were exposed to crizotinib. Autophagy inhibition caused a dramatic decrease in apoptosis in one of the MET-amplified cell lines (MKN45) but not in the other (SNU-5). Because autophagy may provide energy in cells subjected to growth factor deprivation, we explored the effects of MET or autophagy inhibition on cellular ATP levels. This revealed that autophagy-dependent ATP production was selectively required for apoptosis in the MKN45 cells and that chemical ATP depletion mimicked the effects of autophagy inhibition to block cell death. Overall, the data reveal a novel relationship between ATP depletion and resistance to MET inhibitor-induced cell death. Our observations suggest that autophagy inhibitors could have unintended consequences when they are combined with growth factor receptor inhibitors in tumors that require autophagy-dependent ATP production for apoptosis. 12 samples triplicate samples of SNU-5 and MKN45 +/- criztonib for 24 hours

2016-05-13 | E-GEOD-77320 | biostudies-arrayexpress

MicroRNA profiling by array of Enterococcus faecalis infection in human MKN74 gastric adenocarcinoma cell cultures to investigate the effect of bacterial infection on the global microRNA profile

Project description:MKN74 cells were infected with live E. faecalis or with E. faecalis lysate for 5 days.

2014-05-01 | E-MEXP-3694 | biostudies-arrayexpress

Influence of Set7/9 on hESC differentiation

Project description:We analyzed the role of the histone lysine methyltransferase Set7/9 in the differentiation of human embryonic stem (ES) cells. Human ES cell lines expressing a control short hairpin and a short hairpin against Set7/9 were established and the genome wide expression profile was compared between both cell lines at different days during differentiation. Analysis of both profiles indicates that in the absence of Set7/9 there is a delay in the silencing of self-renewal factors as well as in the induction of differentiation markers. These results indicate that Set7/9 plays an active role in the differentiation of human ES cells. control and set7/9 shRNA hESCs were differentiated, and profiling was realized at days 0, 8 and 15.

2016-02-17 | E-GEOD-24768 | biostudies-arrayexpress

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