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

• Published in: Chemical research in toxicology 2021-09, Vol.34 (9), p.2019-2023
• Main Authors: Moyano, Paula, Garcia, José Manuel, García, Jimena, Pelayo, Adela, Muñoz-Calero, Pilar, Frejo, María Teresa, Flores, Andrea, del Pino, Javier
• Format: Article
• Language: English
• Subjects: Basic Helix-Loop-Helix Transcription Factors - agonists; Cell Line, Tumor; Cell Proliferation - drug effects; Chlorpyrifos - toxicity; Cyclooxygenase 2 - metabolism; Dinoprostone - metabolism; Disinfectants - toxicity; Heat-Shock Proteins - metabolism; HSP70 Heat-Shock Proteins - metabolism; HSP90 Heat-Shock Proteins - metabolism; Humans; Rapid Report; Receptors, Aryl Hydrocarbon - agonists; Up-Regulation - drug effects; Wnt Signaling Pathway - drug effects
• ISSN: 0893-228X; 1520-5010
• DOI: 10.1021/acs.chemrestox.1c00258

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.