Fig. 8

The proposed model for ERβ-induced autophagy inhibiting breast cancer cell migration and invasion. In this model, when ERβ bound with ligands (DPN), DPN-ERβ complexes directly bound to the ERE of the CLDN6 promoter and enhanced CLDN6 expression. In addition, activated ERβ can interact with Sp1 and bind the Sp1 transcriptional regulation domains of the CLDN6 promoter to induce CLDN6 expression. ZO-1 and UVRAG act as bridge molecules for the CLDN6-beclin1 interaction. CLDN6 and ZO-1/UVRAG/beclin1 form complexes and serve as a platform for recruiting other autophagy regulatory proteins (atg5, atg16 and LC3-II) and induce autophagy to suppress the migration and invasion of breast cancer cells