〔Abstract〕 Objective To investigate the effect of quercetin(Que) on the expression of claudin 6(CLDN6) and the proliferation, migration and invasion of endometriosis cells, and then analyze its possible mechanism. Methods Forty patients with endometriosis were selected. Endometrial tissue was harvested during operation, and ectopic endometrial stromal cells(EcSCs) were cultured. EcSCs were treated with Que at different concentrations(0, 12.5, 25, 50 μmol/L). The effects of different concentrations of Que on the proliferation of EcSCs were detected by MTT assay. The expressions of proliferating cell nuclear antigen and CLDN6 were detected by Western blot. Transwell migration and invasion assays were used to detect cell migration and invasion. Si-control and si-CLDN6 were transfected into EcSCs, and the effects of silencing CLDN6 expression on the proliferation, migration and invasion of EcSCs were analyzed. Subsequent experiments were divided into 4 groups: NC group, Que group, Que+pcDNA group, Que+pcDNA-CLDN6 group. MTT and Transwell migration and invasion assays were used to detect the proliferation, migration and invasion ability of EcSCs. Western blot was used to detect the expressions of proliferating cell nuclear antigen(PCNA), matrix metalloproteinase-2(MMP-2), MMP-9, epithelial-mesenchymal transitions and integrin-linked kinase(ILK) signaling pathway-related proteins. Results The proliferation, migration and invasion of EcSCs were significantly inhibited by Que, which was dose-dependent and significantly inhibited the expressions of CLDN6, PCNA, MMP-2 and MMP-9. Silencing CLDN6 expression could significantly inhibit the proliferation, migration and invasion of EcSCs. Que could significantly inhibit the expression of N-cadherin, Vimentin, ILK and p-AKT proteins and promote the expression of E-cadherin protein. While transfection of CLDN6 overexpression vector significantly reversed the inhibitory effect of Que on proliferation, migration and invasion of EcSCs. Conclusion Que can significantly inhibit the proliferation, migration and invasion of endometriosis cells by inhibiting the expression of CLDN6, which may inhibit the activation of ILK signaling pathway and EMT transition.