NR4A1 and breast carcinoma: Previous studies in cancer celllines showed that low concentrations of PFOS (1–100 nM) inducedthe proliferation of T47D breast cancer cells; however, the antiestrogenfasoldex inhibited this response, suggesting that the proliferativeactivity was related to the estrogenic activity of PFOS and PFOS alonedid not affect cell growth.58 In contrast,25–200 μM PFOS decreased the growth of A549 lung cancercells,57 and this response would be comparableto that observed for NR4A1 inverse agonists47,63,64 (Figure 2).