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Identification of differential gene expression modulated by knockdown of MUC1 in MKN45 gastric carcinoma cells

ABSTRACT: Transcripts upregulated or downregulated by knockdown of MUC1 were identified through expression profiling of a total of 12,135 genes in comparison with MKN45- MUC1 RNAi clones and control clones.

ORGANISM(S): Homo sapiens

PROVIDER: GSE28975 | GEO | 2011/11/15

SECONDARY ACCESSION(S): PRJNA140489

REPOSITORIES: GEO

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Identification of differential gene expression modulated by knockdown of MUC1 in MKN45 gastric carcinoma cells

Project description:Transcripts upregulated or downregulated by knockdown of MUC1 were identified through expression profiling of a total of 12,135 genes in comparison with MKN45- MUC1 RNAi clones and control clones. We endeavored to identify genes which expression is affected by MUC1 by performing cDNA microarray analysis on two MKN45 MUC1 RNAi clones and one control clone.

2011-11-15 | E-GEOD-28975 | biostudies-arrayexpress

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

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Identification of mRNAs modulated by knockdown of CD24

Project description:We endeavored to identify factors and pathways regulated by CD24 and to obtain leads regarding the mechanism by which CD24 inhibited the invasiveness and metastasis of pancreatic cancer cells by performing cDNA microarray analysis on S2-013 CD24 RNAi clones and control clones. The group of genes showing increased expression was mainly comprised of genes for molecules with functions related to RNA metabolism, transcription factors, proteases, and molecules involved in embryonic development and cell growth. The set of genes downregulated by knockdown of CD24 included the target mRNAs of a phosphorylation-dependent endoribonuclease G3BP that interacted with CD24. The target mRNAs of G3BP were identified in GSE17056. These results suggested that CD24 inhibited the RNase activity of G3BP, and that a function of CD24 was to inhibit the degradation of specific mRNAs. Transcripts upregulated or downregulated by knockdown of CD24 were identified through expression profiling of a total of 12,135 genes in S2-013 CD24 RNAi clones compared to control clones. Before labeling with Cy5 or Cy3, total RNA from two S2-013 CD24 RNAi clones were mixed and total RNA from two control clones were mixed. The supplementary files 'GSE17055_higher_siCD24.txt' and 'GSE17055_higher_control.txt' list the differentially expressed genes.

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Affymetrix miRNA chip showed the differential miRNA expression in TRAIL‐resistant BGC823 and TRAIL‐sensitive MKN45 cells

Project description:In order to explore the effect of miRNA on TRAIL sensitivity of gastric cancer, we selected TRAIL-sensitive MKN45 and TRAIL-resistant BGC823 gastric cancer cell line. The expression of miRNA in MKN45 and BGC823 was detected by miRNA chip. "3" is the miRNA expression file of BGC823. "4" is the miRNA expression file of MKN45.

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Project description:As miRNAs are increasingly shown to be vital regulators of cellular behavior as well as diseases including cancer, it is highly important to identify and characterize miRNAs that are regulated by CUL4B. Here, 106 miRNAs were identified upregulated in MKN45-4BI cells compared with NS cells.

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Anti-proliferation activity of fucoidan on MKN45 gastric cancer cells and downregulation of phosphorylated ASK1, a cell-cycle-regulated cyclin-dependent kinase

Project description:Fucoidan is a high-molecular polysaccharide whose main constituent is sulfated fucose. Extensive studies have demonstrated numerous interesting biological activities for fucoidan. We specifically focused on the anti-proliferation activity of fucoidan and examined the underlying mechanism in MKN45 gastric cancer cells. BrdU assay revealed that fucoidan impeded the MKN45 cell cycle by approximately 50%, and clonogenic assay also showed that fucoidan inhibited cell proliferation. Preliminary examinations of fucoidan using LDH assay showed no immediate cytotoxic effects at 24-h exposure. However, longer time courses revealed inhibition of cell growth at 4 days in a dose-dependent manner. Microarray analysis in MKN45 cells treated with fucoidan identified genes that were upregulated and downregulated in response to fucoidan, including MAP3K5, or ASK1 (apoptosis signal-regulating kinase), which was upregulated by 1.38-fold. Western blot confirmed that fucoidan increased ASK1 protein levels, while reducing the levels of phosphorylated ASK1. Reduction of ASK1 by siRNA decreased proliferation of MKN45 cells. Our findings show that fucoidan may suppress cellular proliferation and DNA synthesis in MKN45 cells by suppressing the ASK1-p38 signaling pathway through reduction of phosphorylated ASK1 levels.

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Impact of MUC1 mucin downregulation in the phenotypic characteristics of MKN45 gastric carcinoma cell line.

Project description: Not available

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Sequencing the anti-MUC1 hybridoma antibody 139H2

Project description:Mucin 1 (MUC1) is a transmembrane mucin expressed at the apical surface of epithelial cells at different mucosal surfaces including breast and intestine. The MUC1 extracellular domain contains a variable number of tandem repeats (VNTR) of 20 amino acids, which are heavily O-linked glycosylated. Monoclonal antibodies against the MUC1 VNTR can be powerful tools because of their multiplicity of binding and possible applications in the diagnosis and treatment of MUC1-expressing cancers. One such antibody is the hybridoma mouse monoclonal 139H2 which is also widely used as a research tool to study non-cancer MUC1. Here we report direct mass spectrometry-based sequencing of hybridoma-derived 139H2 IgG, which enabled reverse engineering of a recombinant 139H2.

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