Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA192899 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
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.
2014-06-20 | GSE45052 | GEO
Project description:Mechanisms of pparγ activation by non-steroidal anti-inflammatory drugs and GQ16.
| PRJNA270064 | ENA
Project description:NSAIDs (non-steroidal anti-inflammatory drugs) inhibit cyclooxygenase (COX) enzymes and prevent Alzheimer’s disease (AD) at preclinical stages in cognitively normal aging populations. We modeled NSAID prevention of memory impairment in AD model mice to identify novel targets of NSAID action. We found that the widely-used NSAID ibuprofen prevented early hippocampus-dependent memory deficits in APP-PS1 mice. We therefore analyzed gene expression in the hippocampus of these mice.
2016-06-14 | GSE67306 | GEO
Project description:The alarming rise of antimicrobial resistance in Mycobacterium tuberculosis coupled with the shortage of new antibiotics has made tuberculosis (TB) control a global health priority. Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the growth of multi-drug resistant isolates of M. tuberculosis. Repurposing NSAIDs, with known clinical properties and safety records, offers a direct route to clinical trials. Therefore we investigated the novel mechanisms of anti-mycobacterial action of the NSAID, carprofen. Integrative molecular and microbiological approaches revealed that carprofen, a bactericidal drug, inhibited bacterial drug efflux mechanisms. In addition, carprofen restricted mycobacterial biofilm-like growth, highlighting the requirement of efflux-mediated communicative systems for the formation of biofilms. Transcriptome profiling revealed that carprofen likely acts by inhibiting respiration through the disruption of membrane potential, which may explain why spontaneous drug-resistant mutants could not be raised due to the pleiotropic nature of carprofen’s anti-tubercular action. This immunomodulatory drug has the potential to reverse TB antimicrobial resistance by inhibiting drug efflux pumps and biofilm formation, and paves a new chemotherapeutic path for tackling tuberculosis.
2020-08-15 | E-MTAB-6191 | biostudies-arrayexpress
Project description:Chronic inflammation plays a critical role in the initiation and development of various human illnesses. The use of steroidal anti-inflammatory drugs (SAIDs) or non-steroidal anti-inflammatory drugs (NSAIDs) is now much more frequent and presents a number of unwanted side effects. For example long- or short-term usage of SAIDs presents multiple negative side effects such as stomach irritation, thinning of the skin, immune defence regression, weight gain and even sometimes a cortico-dependence, and NSAIDs have been linked to a higher risk of strokes, heart attacks, and heart-related deaths. In parallel, there has been renewed interest in alternative medicines and natural therapies and thousands of potential medicinal plants, including sage and chamomile. This study assesses the gene expression responses of human mature adipopcytes (differentiated from fibroblastic pre-adipocytes [PromoCell, Germany; Catalogue #C-12730]), pre-treated with aqueous ethanol extract of sage (Salvia officinalis) or Roman chamomile (Chamaemelum nobile), following 4h or 24h treatment with IL-1B versus control conditions.
2020-10-05 | E-MTAB-9609 | biostudies-arrayexpress
Project description:Chronic inflammation plays a critical role in the initiation and development of various human illnesses. The use of steroidal anti-inflammatory drugs (SAIDs) or non-steroidal anti-inflammatory drugs (NSAIDs) is now much more frequent and presents a number of unwanted side effects. For example long- or short-term usage of SAIDs presents multiple negative side effects such as stomach irritation, thinning of the skin, immune defence regression, weight gain and even sometimes a cortico-dependence, and NSAIDs have been linked to a higher risk of strokes, heart attacks, and heart-related deaths. In parallel, there has been renewed interest in alternative medicines and natural therapies and thousands of potential medicinal plants, including sage and chamomile. This study assesses the gene expression responses of human SK-N-SH neuroblastoma cells, pre-treated with aqueous ethanol extracts of sage (Salvia officinalis) or Roman chamomile (Chamaemelum nobile), following 4h or 24h treatment with IL-1B versus control conditions.
2020-10-05 | E-MTAB-9611 | biostudies-arrayexpress
Project description:We previously showed that doxycycline and carprofen , a veterinary non-steroidal anti-inflammatory drug, have synergistic antimicrobial activity against methicillin-resistant Staphylococus pseudintermedius (MRSP) carrying the tetracycline resistance determinant TetK. To elucidate the molecular mechanism of this synergy, we investigated the effects of the two drugs, individually and in combination, using a comprehensive approach including two-dimensional differential in-gel electrophoresis (2D DIGE).
2020-05-26 | PXD013725 | Pride
Project description:Oxicam-type nonsteroidal anti-inflammatory drugs inhibit NPR1-mediated salicylic acid pathway
| PRJNA646744 | ENA
Project description:This study was undertaken to assess the similarities (or differences) between the well-established PPARγ agonist Rosiglitazone and Non-steroidal anti-inflammatory drugs (NSAIDs) diclofenac, indomethacin and ibuprofen, as well as the partial agonist GQ16 at the transcriptome level. Assessment of NSAID and GQ16 activities in PPARγ-dependent 3T3-L1 cells reveals that NSAIDs and GQ16 display similar effects toward PPARγ-dependent target genes in a manner similar to that of Rosiglitazone.
2015-06-01 | GSE64075 | GEO