Previous study showed that natural estrin, 17Estradiol (E2), could weaken the estrogenicity of Bisphenol A (BPA), a common estrin in water resources. In order to learn the potential mechanisms, experiments were performed with human breast cancer cell MCF7 on the cell cycle, estrogen receptor pathway and MAPKs pathway. Results showed that E2 worked through estrogen receptors and ERK pathway, and activated Cmyc gene, Cfos gene, and cyclin D1 protein, and thus increased the S section of the cell cycle. BPA worked mainly through estrogen receptors by activating cyclin D1 protein, and increased the S and G2 sections of the cell cycle. The mixture of BPA and E2 worked through both pathways, activated both Cfos and cyclin D1, and increased both S and G2 sections of the cell cycle. The main mechanism of E2’s weakening on BPA’s estrogenicity might be the decreased expression of Cmyc protein.