Objective To study the cellular senescence and molecular mechanism of olaparib in MCF-7 breast cancer cells. Methods The effects of olaparib on the proliferation and migration of MCF-7 cells were detected dynamically by real-time cell analysis ( RTCA) technology. The effects of olaparib on the Senescence was detected by using the senescence-associated β-galactosidase (SA-β-gal). Quantitative polymerase chain reaction was used to analyze the effects of olaparib on the expression levels of genes encoding the senescence-associated factors p16, p21, C/ EBP homologous protein, interleukin ( IL )-6, IL-8, plasminogen activator inhibitor 1, phosphatase and tensin homolog deleted on chromosome 10, p27, retinoblastoma gene, Ki67, and E2F1. The effects of olaparib on the expression levels of the senescence-associated proteins p21, γH2AX, pRB, cyclin D1, insulin-like growth factor binding protein 3, and Ki67 were analyzed by Western Blot. Results Olaparib inhibited the proliferation and migration and induced the senescence of MCF7 cells. Long-term (96 h) treatment with olaparib significantly up-regulated the gene expression levels of p16, p21, p27,C/ EBP homologous protein, IL-6, IL-8, plasminogen activator inhibitor 1, phosphatase and tensin homolog deleted on chromosome 10, and retinoblastoma protein (P< 0. 01) and significantly down-regulated the gene expression levels of Ki67 and E2F1 (P< 0. 01) in MCF-7 cells. Olaparib significantly increased protein expression levels of p21, γH2AX, and insulin-like growth factor binding protein 3 in MCF-7 cells (P< 0. 01, P< 0. 01, P< 0. 05) and significantly decreased cyclin D1, pRB, and Ki67 levels (P< 0. 05, P < 0. 01, P< 0. 05). Conclusions Olaparib can inhibit proliferation and migration and induce senescence in MCF-7 breast cancer cells.