In Utero Exposure to Bisphenol a Promotes Mammary Tumor Risk in MMTV-Erbb2 Transgenic Mice Through the Induction of ER-erbB2 Crosstalk

摘要: Bisphenol A (BPA) is the most common environmental endocrine disrupting chemical. Studies suggest a link between perinatal BPA exposure and increased breast cancer risk, but underlying mechanisms remain unclear. This study aims to investigate effects of in utero on mammary tumorigenesis MMTV-erbB2 transgenic mice. Pregnant mice were subcutaneously injected with (0, 50, 500 ng/kg 250 µg/kg BW) daily gestational days 11–19. Female offspring examined for tumorigenesis, puberty onset, morphogenesis, signaling ER erbB2 pathways. In low dose (500 ng/kg) induced earlier terminal end buds, prolonged estrus phase, which was accompanied by proliferative morphogenesis. CD24/49f-based FACS analysis showed that expansion luminal basal/myoepithelial cell subpopulations at PND 35. Molecular tissues 70 doses upregulation ERα, p-ERα, cyclin D1, c-myc, concurrent activation erbB2, EGFR, erbB-3, Erk1/2, Akt, growth factors/ligands. Our results demonstrate promotes through induction ER-erbB2 crosstalk epithelial reprogramming, advance our understanding mechanism associated BPA-induced risk. The studies also support using mouse model relevant studies.