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This study aimed to elucidate the roles and regulatory mechanism of miR-2861 in the development of endometriosis. The expression of miR-2861 in endometriotic tissues and eutopic endometrial tissues was determined. Ectopic endometrial cells were transfected with miR-2861 mimic, miR-2861 inhibitor and their corresponding controls. The effects of miR-2861 overexpression and inhibition on cell proliferation and apoptosis were then investigated. In addition, regulatory relationship between miR-2681 and signal transducer and activator of transcription 3 (STAT3) or matrix metalloproteinase 2 (MMP2) was explored, as well as between STAT3 and MMP2. Compared with eutopic endometrial tissues, miR-2861 was significantly downregulated in endometriotic tissues. Overexpression of miR-2861 markedly inhibited ectopic endometrial cell proliferation and induced apoptosis. Additionally, STAT3 and MMP2 were confirmed as the targets of miR-2861, and the effects of knockdown of STAT3 or MMP2on regulating cell proliferation and apoptosis were opposite with inhibition of miR-2861. Besides, STAT3 could enhance the expression of MMP2 in ectopic endometrial cells. Our study reveals that miR-2861 was lowly expressed in endometriotic tissues, and downregulation of miR-2861 may promote proliferation and inhibit apoptosis of ectopic endometrial cells in endometriosisviaupregulation of STAT3 and MMP2. miR-2861 may be a potential biomarker or therapeutic target for endometriosis.