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Celecoxib induced transcriptional alterations in gastric cancer cells

ABSTRACT: Celecoxib is recognized to have chemopreventive and anti-cancer property beyond its anti-inflammatory function. Celelcoxib treatment in AGS cells down regulates Wnt/β-catenin, STAT3, RXR and ERK/MAPK signaling pathways. Transcriptional profiling after celecoxib shows differential regulation of oncogenic pathway regulated genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE54657 | GEO | 2014/04/01

SECONDARY ACCESSION(S): PRJNA237300

REPOSITORIES: GEO

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Celecoxib induced transcriptional alterations in gastric cancer cells

Project description:Celecoxib is recognized to have chemopreventive and anti-cancer property beyond its anti-inflammatory function. Celelcoxib treatment in AGS cells down regulates Wnt/M-NM-2-catenin, STAT3, RXR and ERK/MAPK signaling pathways. Transcriptional profiling after celecoxib shows differential regulation of oncogenic pathway regulated genes. AGS cell were treated with celecoxib in triplicates and incubated for 24 hours. The processed samples were hybridized in M-bM-^@M-^\HuGene-1_0-stM-bM-^@M-^] array and the differentially expressed genes were taken for pathway analysis and transcription factor enrichment analysis.

2014-04-01 | E-GEOD-54657 | biostudies-arrayexpress

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Chemoprevention of the hepatocarcinogenesis by celecoxib

Project description:Microarray analysis is a useful methodology to identify target genes modulated by anticancer drugs. Here, celecoxib effect on gene expression profiles was evaluated in the modified resistant hepatocyte model. Animals subjected to carcinogenic treatment were fed with diet containing 1500 ppm of celecoxib. Two schemes of celecoxib administration were designed. In the progression protocol, celecoxib was administrated between days 18 and 25 post-cancer initiation, a total of 8 celecoxib treatment days, when well established preneoplastic lesions starts to appear. In the initiation protocol, celecoxib was administrated from one week before until 25 days after of cancer initiation, a total of 32 celecoxib treatment days. A rat group was subjected only to the carcinogenic treatment as cancer positive control. Gene expression profiles of all groups were compared to a negative untreated control. The evaluation of gene expression profiles permitted us to identify new target genes that are modulated by celecoxib treatment. A possible mechanism of celecoxib chemoprevention of hepatocarcinogenesis is proposed.

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Project description:The coxibs are a subset of non-steroidal anti-inflammatory drugs (NSAIDs) that selectively target cyclooxygenase-2 (COX-2) to inhibit prostaglandin signaling and reduce inflammation. However, only celecoxib remains in use, necessitating exploration of broader mechanisms of the coxibs. Here, we report a novel binding site for celecoxib on prostaglandin E synthase (PTGES), an enzyme downstream of COX-2 in the prostaglandin signaling pathway using an isotopically-coded cleavable chelation-assisted biotin probe. Evaluation of the multi-functional probe revealed significantly improved tagging efficiencies attributable to promotion of CuAAC chemistry by the embedded picolyl functional group. Application of the probe within the small molecule interactome mapping by photo-affinity labeling (SIM-PAL) platform using photo-celecoxib as a reporter for celecoxib identified known targets (e.g., carbonic anhydrase 12) and the significant enrichment of PTGES, along with six additional membrane proteins and 15 subunits of the cytochrome complex. In addition, four binding sites to celecoxib were mapped by the probe, including a direct interaction with PTGES. The interaction between celecoxib and PTGES was validated by competitive displacement and thermal shift assay. The binding site between celecoxib and PTGES enabled the development of a structural model of the interaction and will inform the further development of new selective inhibitors of the prostaglandin signaling pathway.

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Rat cardiomyocyte; control vs celecoxib treatment

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