Open AccessAryl 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
Author(s) -
Paula Moyano,
José M. García,
Paula Moyano,
Adela Pelayo,
Pilar Muñoz-Calero,
María Teresa Frejo,
Andrea Flores,
Javier del Pino
Publication year - 2021
Publication title -
chemical research in toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.031
H-Index - 156
eISSN - 1520-5010
pISSN - 0893-228X
DOI - 10.1021/acs.chemrestox.1c00258
Subject(s) - mcf 7 , wnt signaling pathway , aryl hydrocarbon receptor , cell growth , heat shock protein , cancer research , chemistry , breast cancer , microbiology and biotechnology , cell , cancer cell , signal transduction , hsp90 , cancer , biology , medicine , biochemistry , human breast , gene , transcription factor
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.