Endometriosis is a benign disease, but has invasion and metastasis characteristics similar to malignant tumors. Clinically, it is a difficult problem of gynecological clinical treatment for its high recurrence rate. It has been confirmed that miR-363 was downregulated in endometriosis tissues and miR-363 overexpression inhibited the invasion ability of endometrial stromal cells (ESCs). In order to explore the potential mechanism of miR-363-reduced ESC migration and invasion progression, we sought to demonstrate the targeted mRNA expression levels of miR-363 through microarray, and performed cluster analysis to identify potential functions of these targeted genes in ESCs. The wound migration assay showed that there was an observable trend of cell migration potential decrease after transfection with hsa-miR-363. The qRT-PCR result showed that compared to miR-363 negative control cell group, miR-363 was upregulated 3,264.58-fold after miR-363 lentiviral transfection in miR-363 mimics group. The microarray data showed that compared to ESCs miR-363 negative control cell group, 249 genes were upregulated in ESCs miR-363 mimics cells group, and 139 genes were downregulated. Gene Ontology analysis and the pathway analysis data demonstrated that these target genes are mainly involved in cell migration, cell adhesion and invasion, proliferation, apoptosis, alteration of endometrial cells and some related signaling pathways. Our study explored the gene expression pattern after miR-363 overexpression, which could expand the insights into the miR-363 function and molecular mechanisms in endometriosis.