Bisphenol AF promotes estrogen receptor-positive breast cancer cell proliferation through amphiregulin-mediated crosstalk with receptor tyrosine kinase signaling

摘要: Exposure to bisphenol A (BPA), an endocrine-disrupting compound, is associated with increased risk of estrogen-related diseases, including estrogen receptor-positive (ER+) breast cancer. Although analogs, i.e. AF (BPAF), have replaced BPA in industrial settings, increasing data indicate that these alternatives may similar or even more potent estrogenic effects. As such, BPAF exhibits ER binding affinities than biochemical assays. However, preclinical studies exploring the effects on ER+ cancer are missing mechanistic data. Thus, we aimed characterize MCF-7 and T47D cells insight. We found promoted cell growth cycle progression concurrently BPAF-induced ERα transcriptional activity ER-RTK signaling activation. blockage revealed proliferation crosstalk were ER-dependent. Gene expression demonstrated AREG a sensitive target our vitro models. Importantly, determined upregulation necessary for cellular responses. Ultimately, novel finding mediates supports future impact human assess safety profile BPAF.