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Long-term exposure of early-transformed human mammary cells to low-doses of Benzo[a]pyrene and/or Bisphenol-A enhances their cancerous phenotype via an AhR/GPR30 interplay

ABSTRACT: Long-term exposure of early-transformed human mammary cells to low-doses of Benzo[a]pyrene and/or Bisphenol-A enhances their cancerous phenotype via an AhR/GPR30 interplay

PROVIDER: PRJNA595858 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10700801_1.fastq.gz	Fastqsanger.gz
	SRR10700801_2.fastq.gz	Fastqsanger.gz
	SRR10700802_1.fastq.gz	Fastqsanger.gz
	SRR10700802_2.fastq.gz	Fastqsanger.gz
	SRR10700803_1.fastq.gz	Fastqsanger.gz

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Long-term exposure of early-transformed human mammary cells to low-doses of Benzo[a]pyrene and/or Bisphenol-A enhances their cancerous phenotype via an AhR/GPR30 interplay

Project description:We report that long term exposure to BPA and B(a)P enhances cancerous phenotype via an Ahr/GPR30 interplay

2020-04-27 | GSE142073 | GEO

Long-Term Exposure of Early-Transformed Human Mammary Cells to Low Doses of Benzo[a]pyrene and/or Bisphenol A Enhances Their Cancerous Phenotype via an AhR/GPR30 Interplay.

Project description:It is of utmost importance to decipher the role of chronic exposure to low doses of environmental carcinogens on breast cancer progression. The early-transformed triple-negative human mammary MCF10AT1 cells were chronically (60 days) exposed to low doses (10-10 M) of Benzo[a]pyrene (B[a]P), a genotoxic agent, and/or Bisphenol A (BPA), an endocrine disruptor. Our study revealed that exposed MCF10AT1 cells developed, in a time-dependent manner, an acquired phenotype characterized by an increase in cancerous properties (anchorage independent growth and stem-like phenotype). Co-exposure of MCF10AT1 cells to B[a]P and BPA led to a significantly greater aggressive phenotype compared to B[a]P or BPA alone. This study provided new insights into the existence of a functional interplay between the aryl hydrocarbon receptor (AhR) and the G protein-coupled receptor 30 (GPR30) by which chronic and low-dose exposure of B[a]P and/or BPA fosters the progression of MCF10AT1 cells into a more aggressive substage. Experiments using AhR or GPR30 antagonists, siRNA strategies, and RNAseq analysis led us to propose a model in which AhR signaling plays a "driver role" in the AhR/GPR30 cross-talk in mediating long-term and low-dose exposure of B[a]P and/or BPA. Retrospective analysis of two independent breast cancer cohorts revealed that the AhR/GPR30 mRNA expression signature resulted in poor breast cancer prognosis, in particular in the ER-negative and the triple-negative subtypes. Finally, the study identified targeting AhR and/or GPR30 with specific antagonists as a strategy capable of inhibiting carcinogenesis associated with chronic exposure to low doses of B[a]P and BPA in MCF10AT1 cells. Altogether, our results indicate that the engagement of both AhR and GPR30 functions, in particular in an ER-negative/triple-negative context of breast cells, favors tumor progression and leads to poor prognosis.

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Glutathione S-transferase induction after exposure to benzo[a]pyrene

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Benzo(a)pyrene contaminated rhizosphere soil

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Project description:Benzo[a]pyrene is a Group 1 carcinogen. It undergoes metabolism in the liver through CYP1A1 and CYP1B1 enzymes. This study was conducted to investigate the response to benzo[a]pyrene in the liver when these enzymes are knocked down.

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