Background The lacking of estrogen, progesterone and ERBB2 receptor makes the therapy of Triple negative breast cancer (TNBC) is particularly challenging. Accumulating evidences has demonstrated the dysfunction and critical roles of microRNAs (miRNAs) in TNBC. Objective Explore the role of miR-506-3p in TNBC and evaluate the clinical significance of miR-506-3p. Results miR-506-3p expression was significantly decreased in TNBC and correlated with the worst status of TNBC patients. miR-506-3p overexpression repressed the proliferation, migration and induced cell cycle arrest as well as apoptosis of TNBC cells. Mechanistically, SNAI2 was identified as a target of miR-506-3p in TNBC cells. Consistently, SNAI2 was overexpressed in TNBC and inversely correlated with miR-506-3p level. Transfection of SNAI2 abolished the inhibitory role of miR-506-3p in regulating the malignant phenotypes of TNBC cells. Conclusions These results demonstrated the suppressive function of miR-506-3p in TNBC via targeting SNAI2, indicating the possible application of miR-506-3p in TNBC treatment.