Acquired resistance to Taxol (TAX) contributes to clinical treatment failure and significantly reduces the survival rate of patients. The present study aimed to explore the effects of exosomal microRNA (miR)-187-5p on TAX resistance in breast cancer cells and its underlying mechanisms. Exosomes were isolated from MCF-7 and TAX-resistant MCF-7/TAX cells, and the miR-187-5p and miR-106a-3p levels of the cells and exosomes were determined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Next, MCF-7 cells were treated with TAX for 48 h and either treated with exosomes or transfected with miR-187-5p mimics. Cell viability, apoptosis, migration, invasion and colony formation were determined using Cell Counting Kit-8, flow cytometry, Transwell and colony formation assays, and the expression levels of associated genes and proteins were detected by RT-qPCR and western blotting, respectively. Finally, a dual-luciferase reporter gene assay was performed to confirm the target of miR-187-5p. The results showed that miR-187-5p expression levels increased significantly in TAX-resistant MCF-7 cells and exosomes compared with normal MCF-7 cells and exosomes (P<0.05). However, miR-106a-3p was not detected in the cells or exosomes. Therefore, miR-187-5p was selected for subsequent experiments. A series of cell assays showed that TAX inhibited the viability, migration, invasion and colony formation of MCF-7 cells and promoted their apoptosis; however, these changes were reversed by resistant cell exosomes and miR-187-5p mimics. Additionally, TAX significantly upregulated ABCD2 and downregulated β-catenin, c-Myc and cyclin D1, whereas resistant exosomes and miR-187-5p mimics reversed the TAX-induced changes in expression. Finally, ABCD2 was confirmed to directly bind with miR-187-5p. It may be concluded that TAX-resistant cell-derived exosomes delivering miR-187-5p may affect the growth of TAX-induced breast cancer cells by targeting ABCD2 and c-Myc/Wnt/β-catenin signaling.