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Unknown,Transcriptomics,Genomics,Proteomics

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Dichloroacetate (DCA) prevents cisplatin-induced nephrotoxicity without compromising its anti-cancer properties.

ABSTRACT: The aim of this study was to compare the transcriptional changes that occur in the kidneys of mice administered cisplatin or DCA, or both, by RNA-seq. generation of RNA-seq datasets from mice subjected to 4 different treatments. 3 biological replicates per treatment. Saline treatment is control.

ORGANISM(S): Mus musculus

SUBMITTER: Kristine Hardy

PROVIDER: E-GEOD-69652 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Dichloroacetate Prevents Cisplatin-Induced Nephrotoxicity without Compromising Cisplatin Anticancer Properties.

Galgamuwa Ramindhu R Hardy Kristine K Dahlstrom Jane E JE Blackburn Anneke C AC Wium Elize E Rooke Melissa M Cappello Jean Y JY Tummala Padmaja P Patel Hardip R HR Chuah Aaron A Tian Luyang L McMorrow Linda L Board Philip G PG Theodoratos Angelo A

Journal of the American Society of Nephrology : JASN 20160309 11

Cisplatin is an effective anticancer drug; however, cisplatin use often leads to nephrotoxicity, which limits its clinical effectiveness. In this study, we determined the effect of dichloroacetate, a novel anticancer agent, in a mouse model of cisplatin-induced AKI. Pretreatment with dichloroacetate significantly attenuated the cisplatin-induced increase in BUN and serum creatinine levels, renal tubular apoptosis, and oxidative stress. Additionally, pretreatment with dichloroacetate accelerated ...[more]

PMID: 26961349

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Dichloroacetate (DCA) prevents cisplatin-induced nephrotoxicity without compromising its anti-cancer properties.

Project description:The aim of this study was to compare the transcriptional changes that occur in the kidneys of mice administered cisplatin or DCA, or both, by RNA-seq.

2016-03-09 | GSE69652 | GEO

Dehalobacter sp. DCA

Project description:Dehalobacter sp. DCA Genome sequencing

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Exposure of Barrett's associated adenocarcinoma cell lines SKGT4 to deoxycholic acid (DCA)

Project description:The involvment of bile acids such as deoxycholic acid (DCA) in gastro-esophageal reflux disease and subsequent Barrettâs metaplsia has been postulated. This study examines gene expression induced by exposure to DCA in esophageal cells and may be utilised in cross-comparisons with data derived from gene expression studies of Barrettâs esophagus and associated adenocarcinoma. SKGT4 cells were exposed to 300um DCA over 24 hours in duplicate experiments including matched timepoint controls. RNA samples were taken at 4, 8, 12 and 24 hours from DCA (DCA) exposed and resting (REST) timepoint controls.

2010-02-28 | E-GEOD-13376 | biostudies-arrayexpress

Exposure of Barrett's associated adenocarcinoma cell lines SKGT4 to deoxycholic acid (DCA)

2010-02-20 | GSE13376 | GEO

Transcriptome changes triggered by the synthetic defense elicitors DCA and INA in Arabidopsis thaliana

Project description:DCA (3,5-Dichloroanthranilic acid) is a newly identified synthetic defense elicitor. To perform a comparative analysis of defense responses triggered by DCA and the structurally related defense inducer INA (2,6-Dichloroisonicotinic acid) Affymetrix chip experiments were performed with Arabidopsis thaliana seedlings treated with one of these two compounds.

2009-03-20 | GSE13833 | GEO

Exposure of squamous esophageal cell line HET-1A to deoxycholic acid (DCA)

Project description:The involvment of bile acids such as deoxycholic acid (DCA) in gastro-esophageal reflux disease and subsequent Barrettâ??s metaplsia has been postulated. This study examines gene expression induced by exposure to DCA in esophageal cells and may be utilised in cross-comparisions with data derived from gene expression studies of Barrettâ??s esophagus and associated adenocarcinoma. Additionally this study may be used to assess divergence in response to bile acids by comparisons with similar study performed in SKGT4 barrett''s assocaited adenocarcinoma cell line. HET-1A cells were exposed to 300um DCA over 24 hours in duplicate experiments including matched timepoint controls

2010-02-28 | E-GEOD-13378 | biostudies-arrayexpress

Honokiol Bis-Dichloroacetate (Honokiol DCA) Demonstrates Activity in Vemurafenib-Resistant Melanoma in Vivo.

Project description:The majority of human melanomas bears BRAF mutations and thus is treated with inhibitors of BRAF, such as vemurafenib. While patients with BRAF mutations often demonstrate an initial dramatic response to vemurafenib, relapse is extremely common. Thus, novel agents are needed for the treatment of these aggressive melanomas. Honokiol is a small molecule compound derived from Magnolia grandiflora that has activity against solid tumors and hematopoietic neoplasms. In order to increase the lipophilicity of honokiol, we have synthesized honokiol DCA, the dichloroacetate ester of honokiol. In addition, we synthesized a novel fluorinated honokiol analog, bis-trifluoromethyl-bis-(4-hydroxy-3-allylphenyl) methane (hexafluoro). Both compounds exhibited activity against A375 melanoma in vivo, but honokiol DCA was more active. Gene arrays comparing treated with vehicle control tumors demonstrated induction of the respiratory enzyme succinate dehydrogenase B (SDHB) by treatment, suggesting that our honokiol analogs induce respiration in vivo. We then examined its effect against a pair of melanomas, LM36 and LM36R, in which LM36R differs from LM36 in that LM36R has acquired vemurafenib resistance. Honokiol DCA demonstrated in vivo activity against LM36R (vemurafenib resistant) but not against parental LM36. Honokiol DCA and hexafluoro inhibited the phosphorylation of DRP1, thus stimulating a phenotype suggestive of respiration through mitochondrial normalization. Honokiol DCA may act in vemurafenib resistant melanomas to increase both respiration and reactive oxygen generation, leading to activity against aggressive melanoma in vivo.

2016-01-20 | GSE76956 | GEO

Transcription profiling of SKGT4 and HET-1A cell lines exposed to deoxycholic acid (DCA)

Project description:This SuperSeries is composed of the following subset Series: GSE13376: Exposure of Barrett's associated adenocarcinoma cell lines SKGT4 to deoxycholic acid (DCA) GSE13378: Exposure of squamous esophageal cell line HET-1A to deoxycholic acid (DCA) Refer to individual Series

2010-03-02 | E-GEOD-13400 | biostudies-arrayexpress

Exposure of squamous esophageal cell line HET-1A to deoxycholic acid (DCA)

Project description:The involvment of bile acids such as deoxycholic acid (DCA) in gastro-esophageal reflux disease and subsequent Barrett’s metaplsia has been postulated. This study examines gene expression induced by exposure to DCA in esophageal cells and may be utilised in cross-comparisions with data derived from gene expression studies of Barrett’s esophagus and associated adenocarcinoma. Additionally this study may be used to assess divergence in response to bile acids by comparisons with similar study performed in SKGT4 barrett''s assocaited adenocarcinoma cell line.

2010-02-20 | GSE13378 | GEO

DCA-TGR5 signaling activation alleviates inflammatory response and improves cardiac function in myocardial infarction

Project description:The progression of myocardial infarction (MI) involves multiple metabolic disorders. Bile acid metabolites have been increasingly recognized as pleiotropic signalling molecules that regulate multiple cardiovascular functions. G protein-coupled bile acid receptor (TGR5) is one of the receptors sensing bile acids to mediate their biological functions. In this study, we aimed to elucidate the effects of bile acids-TGR5 signaling pathways in myocardial infarction (MI).Mice underwent either the LAD ligation model of MI or sham operation. Both MI and sham mice were gavaged with 10 mg/kg/d DCA or vehicle control since 3-day before the operation. Administration of DCA improved cardiac function at the 3th-day post-MI. The effects of DCA in the heart were determined by RNA-sequencing experiments.

2020-09-24 | GSE158415 | GEO

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