Involvement of JunD in the antiproliferative effect of 9-tetrahydrocannabinol on human breast cancer cells 1
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE8502 | GEO | 2008/12/21
SECONDARY ACCESSION(S): PRJNA101609
REPOSITORIES: GEO
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Project description:THC induces an activation of JunD, by upregulation and translocation to the nuclear compartment, which is accompanied by a decrease in cell proliferation Keywords: THC, JUND Total RNA was isolated from cells treated with vehicle (DMSO), 3 or 5 ïM THC for 8 or 24h, and non-treated cells at the time of drug addition (t=0, reference) using RNeasy Mini Kit (Qiagen, Hilden, Germany). Double strand cDNA was amplify with Superscript Choice System and T7-(deoxythymidine)24 oligo-primers (Life Technologies, Inc., Gaithersburg, MD) and in vitro transcription was carried out with MegascriptTM T7 (Ambion, Austin, TX). For each condition, half of the replicates were labeled with Cy5-dUTP fluorochrome (Amersham, Uppsala, Sweden) and the reference with Cy3-dUTP fluorochrome (Amersham), and the other half were dye swapped. Hybridization was performed on a new version of the Spanish National Cancer Research Center (CNIO) Oncochip manufactured by the CNIO Genomic Unit (http://bioinfo.cnio.es/data/oncochip), which contains 9.726 clones corresponding to 6,386 different genes. Slides were scanned in a Scanarray 5000 XL scanner (GSI Lumonics Kanata, Ontario, Canada) and quantified using the GenePix Pro 6.0 program (Axon Instruments Inc., Union City, CA).
2010-10-08 | E-GEOD-8502 | biostudies-arrayexpress
Project description:THC induces an activation of JunD, by upregulation and translocation to the nuclear compartment, which is accompanied by a decrease in cell proliferation Keywords: THC, JUND Total RNA was isolated from cells treated with vehicle (DMSO), 3 or 5 μM THC for 8 or 24h, and non-treated cells at the time of drug addition (t=0, reference) using RNeasy Mini Kit (Qiagen, Hilden, Germany). Double strand cDNA was amplify with Superscript Choice System and T7-(deoxythymidine)24 oligo-primers (Life Technologies, Inc., Gaithersburg, MD) and in vitro transcription was carried out with MegascriptTM T7 (Ambion, Austin, TX). For each condition, half of the replicates were labeled with Cy5-dUTP fluorochrome (Amersham, Uppsala, Sweden) and the reference with Cy3-dUTP fluorochrome (Amersham), and the other half were dye swapped. Hybridization was performed on a new version of the Spanish National Cancer Research Center (CNIO) Oncochip manufactured by the CNIO Genomic Unit (http://bioinfo.cnio.es/data/oncochip), which contains 9.726 clones corresponding to 6,386 different genes. Slides were scanned in a Scanarray 5000 XL scanner (GSI Lumonics Kanata, Ontario, Canada) and quantified using the GenePix Pro 6.0 program (Axon Instruments Inc., Union City, CA).
| S-ECPF-GEOD-8502 | biostudies-other
Project description:Increased availability of cannabis and cannabinoid-containing products necessitates the need for understanding how exposure to these compounds can affect development. Using cannabinoid receptor-null zebrafish (cnr1-/- and cnr2-/-), we conducted experiments to assess the roles of these receptors in ∆9-tetrahydrocannabinol (THC) and cannabidiol (CBD) developmental and behavioral toxicity. THC increased mortality and deformities (pericardial and yolk sac edemas, a reduction in size) in cnr1-/- and cnr2-/- fish. Conversely, CBD-induced malformations and mortality were significantly reduced in the cnr1-/- and cnr2-/- larvae. THC and CBD exposure caused significantly decreased larval behavior (96 hpf), however, decreased distance travelled was protected in the cnr1-/- and cnr2-/- fish, suggesting these receptors are responsible for mediating behavioral toxicity. Transcriptomic profiling in cnr+/+ embryos developmentally exposed to 4 μM THC or 0.5 μM CBD revealed that a significant portion of differentially expressed genes were targets of PPARγ, a predicted upstream regulator. In Cnr-positive embryos, co-exposure to the PPARγ inhibitor GW9662 and THC or CBD, there was increased toxicity compared to exposure with THC or CBD alone. Co-treatment in the cnr2-/- fish with GW9662 did not alter the CBD-induced decrease in activity. However, co-treatment with GW9662 did remove the protective effect observed in cnr1-/- fish treated to CBD alone. Collectively, these results indicate that PPARγ, Cnr1, and Cnr2 all play crucial roles in the developmental toxicity of THC and CBD.
2021-01-01 | GSE164128 | GEO
Project description:Cigarette smoke (CS)-induced airway inflammation is an important pathologic feature of chronic obstructive pulmonary disease (COPD). Recent studies suggest a potential role of JunD in the regulation of inflammation, but its role in CS-induced airway inflammation has not been reported. This study aimed to determine its role in CS-induced airway inflammation through bioinformatics analysis and in vitro and in vivo experiments. Data from the Gene Expression Omnibus (GEO) database (GSE37147) were analyzed using weighted gene co-expression network analysis (WGCNA) and key driver analysis (KDA), and these analyses were validated using the GSE47460 dataset. The effect of CS on JunD expression was examined in lung tissues of COPD patients and CS-exposed mice and in CS extract (CSE)-exposed BEAS-2B cells. The effects of CSE on airway epithelial inflammatory injury after JunD knockdown or overexpression were also investigated. mRNA-seq and chromatin immunoprecipitation (ChIP)-seq were used to explore the mechanism of JunD-mediated CS-induced airway inflammation. Mice were injected with adeno-associated virus serotype 9 (AAV9)-JunD vector or control vector and then exposed to CS for 4 weeks, and lung tissue morphology and airway inflammation were evaluated. KDA of the lung function-related gene modules in GSE37147 revealed a potential role of JunD in COPD, which was validated in GSE47460. JunD was downregulated in lung tissues of COPD patients and CS-exposed mice and in BEAS-2B cells. JunD knockdown aggravated CSE-induced tumor necrosis factor (TNF)-α and interleukin (IL)-1β release by BEAS-2B cells, while JunD overexpression attenuated these effects. mRNA-seq and ChIP-seq identified several JunD-regulated genes, which are involved in the immune response and TNF signaling pathway and are commonly dysregulated in cell models of airway inflammation. In vivo, JunD overexpression attenuated the CS-induced inflammatory cell infiltration and inflammatory cytokine release in mouse lungs. Thus, JunD is involved in CS-induced airway inflammation and JunD-based therapy may be useful in CS-induced airway disorders.
2020-12-09 | GSE162902 | GEO
Project description:RNA-seq performed in Min6 cells during glucolipotoxicity after CRISPR-mediated depletion of JunD
2019-08-16 | GSE115239 | GEO
Project description:RNA-seq following JunD depletion
| PRJNA474228 | ENA
Project description:Rattus norvegicus Jund, JunD proto-oncogene, AP-1 transcription factor subunit [Source:RGD Symbol;Acc:2945], is differentially expressed in 26 experiment(s);
| ENSRNOG00000019568 | ExpressionAtlas
Project description:Rattus norvegicus Jund, JunD proto-oncogene, AP-1 transcription factor subunit [Source:RGD Symbol;Acc:2945], is expressed in 5 baseline experiment(s);
| ENSRNOG00000019568 | ExpressionAtlas
Project description:Macaca mulatta JUND, JunD proto-oncogene, AP-1 transcription factor subunit [Source:HGNC Symbol;Acc:HGNC:6206], is expressed in 3 baseline experiment(s);
| ENSMMUG00000038371 | ExpressionAtlas
Project description:Homo sapiens JUND, JunD proto-oncogene, AP-1 transcription factor subunit [Source:HGNC Symbol;Acc:HGNC:6206], is differentially expressed in 218 experiment(s);
| ENSG00000130522 | ExpressionAtlas