Xenopus laevis
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ABSTRACT:
PROVIDER: PRJNA117383 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Comparison of expression profiles detected in A549 cells exposed to DMSO, TCDD, and BaP for 2w Exposure to persistent ligands of aryl hydrocarbon receptor (AhR) has been found to cause lung cancer in experimental animals and lung adenocarcinomas are often associated with enhanced AhR expression and aberrant AhR activation. In order to better understand the action of toxic AhR ligands in lung epithelial cells, we performed global gene expression profiling in order to analyse TCDD- induced changes in A549 transcriptome, and compare them with changes in transcriptome of A549 cells exposed to BaP for 2w.
2019-09-01 | GSE122733 | GEO
Project description:The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that binds pollutants, therapeutic drugs and endogenous ligands. The AHR is expressed in all breast cancer subtypes and it can switch the aggressiveness of breast cancer cells from low to high depending on the ligand that it binds. Jagged 1 (JAG1) is a NOTCH receptor ligand that is overexpressed in basal-like breast cancer. JAG1 promotes breast cancer progression in part by increasing the migratory and invasive activity of breast cancer cells (BCCs). The regulation of JAG1 by AHR in MCF-7 and MDA-MB-231 BCCs by two AHR ligands (TCDD and ITE) was investigated in this report. TCDD is the prototype AHR ligand, and ITE is a non-toxic endogenous AHR ligand with anti-cancer activity. Ingenuity pathway analysis (IPA) revealed a significant association between TCDD-regulated genes (TRGs) and cell movement. Short interfering RNA (siRNA)-directed knockdown of AHR confirmed TCDD-stimulated decreases in JAG1 required AHR expression. TCDD-induced reductions in JAG1 were inhibited by the AHR antagonist CH-223191. The endogenous non-toxic AHR ligand ITE also reduced JAG1 by activating AHR in BCCs. MDA-MB-231 are basal-like BCCs that are highly migratory and invasive, and these cancer cell attributes were significantly inhibited by ITE. We reduced JAG1 with targeting siRNA, and the outcome mirrored ITE, it suppressed TNBC cell migration and invasive activity. Collectively, these findings are the first showing that ITE is a tumor-suppressing AHR ligand in TNBC cells in part because it reduces JAG1 expression
2018-08-15 | GSE98514 | GEO
Project description:African clawed frog (Xenopus laevis) is an important model organism for cell and developmental biology.
| PRJNA10707 | ENA
Project description:Responsiveness of a premetamorphic Xenopus tadpole brain to hydroxylated PCBs
| PRJNA131575 | ENA
Project description:Background: Estrogen receptor (ERα) and aryl hydrocarbon receptor (AHR) are two nuclear receptors involved in regulating gene expression. ERα and AHR are regulated by estradiol(E2) and TCDD respectively. They are also regulated by dietary ligands including 3,3´diindolylmethane (DIM) and resveratrol (RES). DIM is an ERα and AHR agonist, while RES is an ERα agonist and AHR antagonist. Few studies have investigated the impact of RES and DIM on ERα and AHR signaling at a genome-wide level. This study assessed ERα and AHR binding and associated gene expression changes after treatment of MCF-7 human breast cancer cells with DIM, RES, E2, TCDD, and E2+TCDD for 1 hour and 6 hours before ChIP and RNA sequencing respectively. Results: 88% and 86% of the ERα bound sites after RES and DIM overlapped with E2 ERα sites. RES and DIM resulted in 577 and 446 differentially expressed genes (DEGs) respectively compared to 866 after E2. 68% and 62.3% of the DEGs after RES and DIM were closest to an ERα binding site. Motif analysis indicated enrichment for AHRE motif among DIM ERα sites but not among E2 or RES ERα sites. Both DIM and E2+TCDD resulted in greater genome wide binding of AHR than TCDD. DIM and E2+TCDD resulted in 10546 and 8904 AHR and ERα co-occupied sites respectively. While co-occupied sites for both enriched for the AHR and ERE motif among others, DIM mediated co-occupied sites enriched for Tcfcp2l1, Tgif1, Gata3 motifs while E2+TCDD mediated ones enriched for the NF1 and Ppara motifs. Overlap of coregulated DEGs after DIM and E2+TCDD indicated 123 were the same among both with 81 and 85 unique coregulated DEGs respectively. Enrichment analysis indicated that more enrichment terms were different than similar for coregulated genes after E2+TCDD and DIM. Conclusions: AHR activation is responsible for DIM mediated reduced regulation of gene expression by ERα relative to E2 and only a subset of the DEG’s after DIM and RES are ERα targets indicating future studies into other transcription factors regulated by DIM and RES are needed for insights into the regulation of gene expression by these ligands.
2023-10-16 | GSE232234 | GEO
Project description:Comparison of expression profiles detected in A549 cells exposed to DMSO, TCDD, CH223191 or their combination Exposure to persistent ligands of aryl hydrocarbon receptor (AhR) has been found to cause lung cancer in experimental animals and lung adenocarcinomas are often associated with enhanced AhR expression and aberrant AhR activation. In order to better understand the action of toxic AhR ligands in lung epithelial cells, we performed global gene expression profiling in order to analyse TCDD- induced changes in A549 transcriptome, both sensitive and non-sensitive to co-treatment with AhR inhibitor CH223191. Comparison of our data with results from previously reported microarray and ChIP-seq experiments enabled us i) to identify candidate genes, which expression status acutely (e.g. Aldh1a3, Grem1, Hipk2, Tiparp), or with a delay (Cdh1, Dkk1, Bmp6), reflects exposure of lung cancer cells to TCDD, ii) to predict processes/pathways (e.g. ER stress, Wnt/β-cat, IFNɣ, EGFR/Erbb1), as well as iii) putative TFs (e.g. Stat, AP1, E2F1, TCF4), which may be implicated in adaptive response of lung cells to TCDD-induced AhR activation.
2018-01-25 | GSE109576 | GEO
Project description:Starting with our early global expression analyses of TCDD-treated human hepatoma cells {Puga, 2000 4679 /id}, the AHR transcriptional induction profile has been extensively studied, whether activated by TCDD, B[a]P or in the absence of exogenous ligands (reviewed in {Frericks, 2007 5618 /id}). In addition to using prior knowledge to integrate expression profiles into the AHR gene target network, we performed a new set of expression profile analyses of wild type Hepa-1c1c7 and c35 cell lines and compared the responses in naïve cells with responses in TCDD or B[a]P exposed cells for 8 hours. Results of our expression array studies are in close agreement with current knowledge. Experiment Overall Design: Three biological replicates were each performed for wildype naïve cells (DMSO), TCDD activated cells, and B[a]P activated cells, and for c35 (AHR mutant) naïve cells (DMSO), TCDD activated cells, and B[a]P activated cells.
2009-04-25 | E-GEOD-11796 | biostudies-arrayexpress
Project description:Comprehensive RNA-seq experiments to measure the expression of homoeologs across different tissues, as a part of the Xenopus laevis genome project. This work is funded by Agency Japanese Ministry of Education, Culture, Sports, Science and Technology (MEXT; "Genome Science" Grant ID 221S0002). Collect mRNA from whole tissue; two female frogs were used as donors for most tissues (Taira dataset for one frog, Ueno dataset for the other frog); testis samples were collected from two male frogs (sibling of two female donors)
2016-10-24 | E-GEOD-73419 | biostudies-arrayexpress
Project description:Over activation of the aryl hydrocarbon receptor (AhR) by TCDD results ampng other phenotypes in severe thymic atrophy accompanied by immunosuppression. The link between thymic atrophy, skewed thymocyte differntiation and immunosuppression is still not fully resolved. This study investigates the TCDD elicted exprssion changes in the ET, cortical thymus epithelial cell line. Keywords: TCDD, AhR, thymic epithelial cells, thymic involution, thymus atrophy
2008-12-31 | GSE10168 | GEO
Project description:Abstract: Inhibitory crosstalk between estrogen receptor alpha (ERalpha) and aryl hydrocarbon receptor (AHR) regulates 17β-estradiol (E2)-dependent breast cancer cell signalling. ERalpha and AHR are transcription factors activated by E2 and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) respectively. Dietary ligands resveratrol (RES) and 3,3´diindolylmethane (DIM) also activate ERalpha while only DIM activates AHR and RES represses it. DIM and RES are reported to have anti-cancer and anti-inflammatory properties. Studies with genome wide targets and AHR and ERalpha regulated genes after DIM and RES are unknown. We used chromatin immunoprecipitation with high-throughput sequencing and transcriptomics to study ERalpha as well as AHR coregulation in MCF-7 human breast cancer cells treated with DIM, RES, E2 or TCDD alone or E2+TCDD for 1 and 6 hours respectively. ERalpha bound sites after DIM enriched for the AHR motif but not after E2 or RES while AHR bound sites after DIM and E2+TCDD enriched for the ERE motif but not after TCDD. More than 90% of the differentially expressed genes closest to an AHR binding site after DIM or E2+TCDD also had an ERalpha site and 60% of coregulated genes between DIM and E2+TCDD were common. Collectively our data shows that RES and DIM differentially regulate multiple transcriptomic targets via ERalpha and ERalpha/AHR coactivity respectively, which need to be considered to properly interpret their cellular and biological responses. These novel data also suggest that when both receptors are activated, ERalpha dominates with preferential recruitment of AHR to ERalpha target genes.
2023-10-16 | GSE232233 | GEO