Diverse studies have shown that miR-155 is overexpressed in different tumor types. However, the precisemolecular mechanism of the ectopic expression of miR-155 in breast cancer is still poorly understood. Tofurther explore the role of miR-155 in breast tumorigenesis, we here assessed the influence of miR-155 antisenseoligonucleotide (miR-155 ASO) on MDA-MB-157 cell viability and apoptosis in vitro. Furthermore, the effectsof inhibitory effects of miR-155 on the growth of xenograft tumors in vivo were determined with performanceof immunohistochemistry to detect expression of caspase-3, a pivotal apoptosis regulatory factor, in xenografts.Transfection efficiency detected by laser confocal microscope was higher than 80%. The level of miR-155expression was significantly decreased (P<0.05) in the cells transfected with miR-155 ASO, compared withthat in cells transfected with a negative control. After being transfected with miR-155 ASO, the viability ofMDA-MB-157 cells was reduced greatly (P<0.05) and the number of apoptotic cells was increased significantly.Additionally, miR-155 ASO inhibited the growth of transplanted tumor in vivo and significantly increased theexpression of caspase-3. Taken together, our study revealed that miR-155 ASO can induce cell apoptosis andinhibit cell proliferation in vitro. Moreover, miR-155 ASO could significantly repress tumor growth in vivo,presumably by inducing apoptosis via caspase-3 up-regulation. These findings provide experimental evidencefor using miR-155 as a therapeutic target of breast carcinoma.