Objective To investigate the molecular mechanism by which miR-93-5p promotes the invasion and migration of triple negative breast cancer (TNBC) cells. Methods The miR-93-5p and faciogenital dysplasia-5 (FGD5) were screened out by Gene Expression Omnibus (GEO). Bioinformatics software was used to predict the candidate target genes for miR-93-5p. The relative expression of miR-93-5p in cells was detected by real-time quantitative PCR. Western blot was used to detect the relative expression of FGD5. TranswellTM assay was performed to detect the effects of miR-93-5p on the invasion and migration of MDA-MB-231 cells. The expression of FGD5 and survival curve in breast cancer and the correlation between miR-93-5p and FGD5 were analyzed by bioinformatics database. Dual luciferase reporter gene experiment was employed to verify the targeting relationship between miR-93-5p and FGD5. Results The miR-93-5p was highly expressed in TNBC tissues and cell lines. The higher the expression of miR-93-5p was, the worse the prognosis of breast cancer patients were. Knockdown of miR-93-5p inhibited the invasion and migration ability of MDA-MB-231 cells. Bioinformatics analysis showed that there were complementary sequences between miR-93-5p and FGD5. FGD5 presented low expression in breast cancer tissues and lower FGD5 expression in breast cancer patients corresponded to poorer prognosis. The expression levels between miR-93-5p and FGD5 were negatively correlated. Transfection of miR-93-5p inhibitor plasmid up-regulated the expression of FGD5 in TNBC cells. Dual luciferase reporter gene experiments confirmed that miR-93-5p could down-regulate the luciferase activity of wild-type FGD5. Conclusion The miR-93-5p can promote the invasion and migration of TNBC cells by targeting FGD5.