Expression profiling of MCF-7 cells with treatment of TCDD
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA385317 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3089090_1.fastq.gz | Fastqsanger.gz | |||
| SRR3089090_2.fastq.gz | Fastqsanger.gz | |||
| SRR3089091_1.fastq.gz | Fastqsanger.gz | |||
| SRR3089091_2.fastq.gz | Fastqsanger.gz | |||
| SRR3089084_1.fastq.gz | Fastqsanger.gz |
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Project description:The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that is regulated by environmental toxicants that function as AHR agonists such as 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD). L-Type Amino Acid Transporter 1 (LAT1) is a leucine uptake transporter that is overexpressed in cancer. The regulation of LAT1 by AHR in MCF-7 and MDA-MB-231 breast cancer cells (BCCs) was investigated in this report. Ingenuity pathway analysis (IPA) revealed a significant association between TCDD-regulated genes (TRGs) and molecular transport. Overlapping the TCDD-RNA-Seq dataset in this report with a published TCDD-ChIP-seq dataset identified that LAT1 was a direct TCDD/AHR gene target. Short interfering RNA (siRNA)-directed knockdown of AHR confirmed that TCDD-stimulated increases in LAT1 mRNA and protein required AHR. TCDD-stimulated increases in LAT1 mRNA was also inhibited by the AHR antagonist CH-223191. Upregulation of LAT1 by TCDD coincided with increases in leucine uptake by MCF-7 cells in response to TCDD. Chromatin immunoprecipitation-quantitative PCR (ChIP-qPCR) assays revealed increases in AHR, AHR nuclear translocator (ARNT) and p300 binding and histone H3 acetylation at an AHR binding site in the LAT1 gene in response to TCDD. In MDA-MB-231 cells, which exhibit high levels of endogenous AHR activity, the levels of endogenous LAT1 mRNA and protein were reduced in response to knockdown of AHR with AHR-siRNA. The regulation of LAT1 by AHR stimulated MDA-MB-231 proliferation. Collectively, these findings have provided a deeper mechanistic understanding of extrinsic and intrinsic regulation of LAT1 by AHR.
2016-05-26 | GSE76608 | 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
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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.
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Project description:We performed ribosome profiling (RIBO-seq) and transcriptome profiling (RNA-seq) to monitor RNAs associated with ribosome in the MCF-7 cell model Keywords: ribosome profiling, translation, MCF-7
2018-07-13 | GSE111866 | GEO
Project description:Global gene expression profiling in A549 cells exposed to TCDD, CH223191 or TCDD+CH223191 for 6 h
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Project description:2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental contaminant. Previous reports revealed TCDD activating aryl hydrocarbon receptor (AhR) pathway and causing cardiac damage. However, the mechanism of AhR-induced cardiac defect in response to TCDD exposure remains unclear. In this study, we characterized the impacts of TCDD exposure on heart morphology and cardiac function in zebrafish. To investigate the differentially expressed genes under TCDD exposure, we collected the zebrafish larave heart from the control and TCDD treatment groups. We then performed gene expression profiling analysis using data obtained from RNA-seq. Transcriptomic profiling showed that, along with an upregulation of the AhR signaling pathway by TCDD, the expression of pro-ferroptosis genes was upregulated, while genes implicated in glutathione metabolism were downregulated. Consistently, lipid peroxidation, as indicated by malonaldehyde (MDA) production, increased in TCDD-exposed cardiac tissue. Accordingly, inhibiting lipid peroxidation with Liproxstatin-1 reversed the adverse cardiac effects under TCDD treatment. Together, our findings demonstrate that AhR-mediated lipid peroxidation contributes to the cardiac developmental defects of TCDD during zebrafish early development.
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