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CDC42 expression is altered by dioxin exposure and mediated by multilevel regulations via AhR in human neuroblastoma

Tuan Xu1,2, Heidi Q Xie1,2, Yunping Li1,2

  • 1State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing, 100085, China.

Scientific Reports
|September 2, 2017
PubMed

Insights

Dioxin exposure alters microRNA (miR) expression in neuroblastoma cells, specifically upregulating hsa-miR-608 and Cell Division Cycle 42 (CDC42). The aryl hydrocarbon receptor (AhR) mediates these dioxin-induced changes.

Area of Science:

  • Neuroscience
  • Toxicology
  • Molecular Biology

Background:

  • Dioxins are environmental pollutants known to disrupt microRNA (miR) expression in various cells.
  • The impact of dioxins on microRNA expression within neuronal cells remains largely uncharacterized.
  • Understanding these effects is crucial for assessing potential neurotoxic risks associated with dioxin exposure.

Purpose of the Study:

  • To investigate the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on microRNA expression in human neuroblastoma cells.
  • To identify specific microRNAs and their target genes involved in the cellular response to TCDD.
  • To elucidate the role of the aryl hydrocarbon receptor (AhR) in mediating TCDD's effects on neuronal gene expression.

Main Methods:

  • Microarray analysis to screen for differentially expressed miRs in TCDD-treated SK-N-SH neuroblastoma cells.
  • Quantitative real-time PCR to validate TCDD-induced changes in specific miR and mRNA expression.
  • Bioinformatics analysis to predict miR targets and associated pathways.
  • Luciferase reporter assays and transfection with miR inhibitors to confirm gene regulation mechanisms.
  • Treatment with an aryl hydrocarbon receptor (AhR) antagonist (CH223191) to assess AhR involvement.

Main Results:

  • TCDD treatment (10-10 M) significantly altered the expression of 277 miRs in SK-N-SH cells, with 53 miRs showing >0.4-fold change.
  • TCDD induced the expression of hsa-miR-608, a primate-specific miR linked to brain functions.
  • TCDD also upregulated the expression of Cell Division Cycle 42 (CDC42), a predicted target of hsa-miR-608, involving both transcriptional and post-transcriptional regulation.
  • The AhR antagonist CH223191 blocked TCDD-induced changes in hsa-miR-608 and CDC42 expression, confirming AhR mediation.

Conclusions:

  • TCDD exposure dysregulates microRNA expression in human neuroblastoma cells.
  • Hsa-miR-608 and its target CDC42 are key players in the neuronal response to TCDD.
  • The aryl hydrocarbon receptor (AhR) is essential for mediating both the transcriptional induction of CDC42 and the post-transcriptional regulation of CDC42 by hsa-miR-608 in dioxin-exposed neuroblastoma cells.

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