Context: Progesterone resistance in the eutopic endometrium(EuE) is suggested to be a critical factor of decreased endometrial receptivity and implantation failure in endometriosis of women of reproductive age. Altered expression of miRNAs has been reported to play an important role in the pathophysiology of endometriosis associated infertility. Objective: To explore the role of miR-194-3p in progesterone receptor (PR) and decidualization in EuE from a subset of women with mild or minimal endometriosis. Methods: The differential expressions of miR-194-3p and PR between endometriosis group and control were validated by quantitative real-time PCR(qRT-PCR). Bioinformatics analysis predicted that miR-194-3p targets the PR 3â€²-untranslated region (UTR). The regulation and functional role of miR-194-3p in PR expression and decidualization were investigated in endometrial stromal cells (ESCs). Patient(s): 19 infertile women with mild or minimal endometriosis (according to the r-AFS classification) and 14 disease-free control subjects. Intervention(s): Endometrium tissue collection, qRT-PCR, cell culture, miRNA transfection, western blotting, luciferase reporter assays, and in vitro decidualization of isolated ESCs. Main Outcome Measure(s): The expression of miR-194-3p and PR mRNAs; the relationship and effect of miR194-3p on PR expression were measured in eutopic ESCs and 293T cells. Result(s): MiR-194-3p expression was increased in mid-secretory EuE of women with mild or minimal endometriosis compared with controls. PR protein levels were inhibited by transfection of ESCs with a miR-194-3p mimic and upregulated by miR-194-3p inhibition. The 3â€² UTR luciferase assay indicated the regulation of PR expression by miR-194-3p. Furthermore, miR-194-3p overexpression inhibited the in vitro decidualization of ESCs. Conclusions: Our study demonstrates that miR-194-3p contributes to the progesterone resistance in endometriosis hindering fertility by repressing the levels of PR and decidualization in EuE. MiR-194-3p regulation emerges as a future therapeutic strategy for endometriosis.