Aryl Hydrocarbon Receptor Activation Produces Heat Shock Protein 90 and 70 Overexpression, Prostaglandin E2/Wnt/β-Catenin Signaling Disruption, and Cell Proliferation in MCF-7 and MDA-MB-231 Cells after 24 h and 14 Days of Chlorpyrifos Treatment

Chem Res Toxicol. 2021 Sep 20;34(9):2019-2023. doi: 10.1021/acs.chemrestox.1c00258. Epub 2021 Aug 23.

Abstract

The biocide chlorpyrifos (CPF) was described to increase breast cancer risk in humans, to produce breast cancer in animals, and to induce cell proliferation in MCF-7 and MDA-MB-231 cells after 1 and 14 days of treatment. The entire mechanisms related to these CPF actions remain unknown. CPF induced cell proliferation in MCF-7 and MDA-MB-231 cells after 1 and 14 days of treatment by AhR activation through the PGE2/Wnt/β-catenin pathway and HSP90 and HSP70 overexpression. Our results reveal new information on CPF toxic mechanisms induced in human breast cancer cell lines, which could assist in elucidating its involvement in breast cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Basic Helix-Loop-Helix Transcription Factors / agonists*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • Chlorpyrifos / toxicity*
  • Cyclooxygenase 2 / metabolism
  • Dinoprostone / metabolism
  • Disinfectants / toxicity*
  • HSP70 Heat-Shock Proteins / metabolism
  • HSP90 Heat-Shock Proteins / metabolism
  • Heat-Shock Proteins / metabolism*
  • Humans
  • Receptors, Aryl Hydrocarbon / agonists*
  • Up-Regulation / drug effects
  • Wnt Signaling Pathway / drug effects*

Substances

  • AHR protein, human
  • Basic Helix-Loop-Helix Transcription Factors
  • Disinfectants
  • HSP70 Heat-Shock Proteins
  • HSP90 Heat-Shock Proteins
  • Heat-Shock Proteins
  • Receptors, Aryl Hydrocarbon
  • Cyclooxygenase 2
  • Chlorpyrifos
  • Dinoprostone