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Change in gene expression of a canine melanoma cell line caused by exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) .

ABSTRACT: Nonsteroidal anti-inflammatory drugs (NSAIDs) has been suggested as adjunctive anti-tumor agents in human and veterinary medicine. However, its anti-tumor molecular machinery is still controversial. Therefore, we performed whole transcriptome analysis to discover gene expression influenced by NSAIDs treatment. A canine melanoma cell line (Mi/CMM1) was treated by three NSAIDs, piroxicam, carprofen, and robenacoxib, at their half maximal (50%) inhibitory concentrations (116 ÂµM, 779 ÂµM, and 156 ÂµM) for 6 hours. Subsequently, total RNA were extracted and microarray analysis was performed to evaluate change in gene expression caused by NSAIDs treatment. Each condition had three biological replicates.

ORGANISM(S): Canis lupus familiaris

SUBMITTER: Kohei Saeki

PROVIDER: E-GEOD-78988 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Change in gene expression of a canine melanoma cell line caused by exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) .

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Sirtuin 3 is a common target of non-steroidal anti-inflammatory drugs to induce gastric cancer cell death and gastric mucosal injury II.

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Project description:Severe malaria encompasses a range of syndromes manifesting systemically or in diverse organs. These are believed to represent the end-stage processes of local parasite sequestration and inflammatory cascades. Classical anti-malarial drugs target parasites only. In treatment of severe disease, adjunctive therapies capable of controlling the inflammatory processes could be beneficial. Innate defense regulator (IDR) peptides display multiple immune modulatory activities. In this study, we assessed peptide IDR-1018, which shows promise as an anti-inflammatory drug, as a lead candidate for adjunctive host-directed therapy of established disease in the P. berghei ANKA model of experimental cerebral malaria (ECM). Intravenously administered IDR-1018 partially protected mice from ECM both prophylactically and in adjunctive treatment with classical anti-malarial drugs. We used transcriptional data from spleens and brains taken early in infection (day 3) of prophylactically treated mice to investigate the protective mechanisms. The microarrays compared spleens and brains from nine IDR-1018 i.v. treated, infected mice (IDR-1018-treated infected) with three saline i.v. treated infected mice (saline-treated infected) and three uninfected untreated control mice (controls). RNA samples were hybridized in randomized order to five Illumina WG-6 v2 BeadChips . No technical replicates were performed.

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2024-01-19 | PXD047236 | Pride

Canis lupus familiaris

Project description:Change in gene expression of a canine melanoma cell line caused by exposure to nonsteroidal anti-inflammatory drugs (NSAIDs) .

| PRJNA314582 | ENA

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Profound chemopreventative effects of a hydrogen sulfide-releasing NSAID in the APCMin/+ mouse model of intestinal tumorigenesis

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2016-01-20 | E-GEOD-76928 | biostudies-arrayexpress

Non-steroidal Anti-inflammatory Drugs Decrease E2F1 Expression and Inhibit Cell Growth in Ovarian Cancer Cells

Project description:Epidemiological studies have shown that the regular use of non-steroidal anti-inflammatory (NSAIDs) drugs is associated with a reduced risk of various cancers. In addition, in vitro and experiments in mouse models have demonstrated that NSAIDs decrease tumor initiation and/or progression of several cancers. However, there are limited preclinical studies investigating the effects of NSAIDs in ovarian cancer. Here, we have studied the effects of two NSAIDs, diclofenac and indomethacin, in ovarian cancer cell lines and in a xenograft mouse model. Diclofenac and indomethacin treatment decreased cell growth by inducing cell cycle arrest and apoptosis. In addition, diclofenac and indomethacin reduced tumor volume in a xenograft model of ovarian cancer. To identify possible molecular pathways mediating the effects of NSAID treatment in ovarian cancer, we performed microarray analysis of ovarian cancer cells treated with indomethacin or diclofenac. Interestingly, several of the genes found downregulated following diclofenac or indomethacin treatment are transcriptional target genes of E2F1. E2F1 was downregulated at the mRNA and protein level upon treatment with diclofenac and indomethacin, and overexpression of E2F1 rescued cells from the growth inhibitory effects of diclofenac and indomethacin. In conclusion, NSAIDs diclofenac and indomethacin exert an anti-proliferative effect in ovarian cancer in vitro and in vivo and the effects of NSAIDs may be mediated, in part, by downregulation of E2F1. The serous ovarian adenocarcinoma cell lines HEY, OVCAR5 and UCI-101 were grown in culture then seeded in 60 mm dishes and treated for 24 hours with 300 mM diclofenac, indomethacin or no treatment (Control). RNA was isolated and one sample from each group was labeled and hybridized to Illumina Sentrix bead arrays.

2014-06-20 | E-GEOD-45052 | biostudies-arrayexpress

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