Objective To study the performance and related molecular mechanism of Olaparib-induced senescence in MCF-7 breast cancer cells. Methods Real-time cell analysis (RTCA) was used to dynamically detect anti-proliferation and anti-migration activities in real time. Senescence-associated β-galactosidase (SA-β-gal) staining was used to observe the senescence-inducing activity of cells. The effects of olaparib on the expression of senescence-associated genes p16INK4a, p21, C/EBP homologous protein (CHOP) , interleukin (IL) -6, IL-8, plasminogen activator inhibitor 1 (PAI-1) , phosphatase and tensin homolog deleted on chromosome 10 (PTEN) , p27, retinoblastoma protein (RB1) , Ki67 and E2F1 were analyzed by qPCR. The effects of olaparib on the expression of senescence-associated proteins p21, γH2AX, pRB, cyclin D1, insulin-like growth factor binding protein 3 (IGFBP3) and Ki67 were analyzed by Western blot. Results Olaparib could inhibit the proliferation and migration of MCF-7 breast cancer cells and induce the senescence of MCF-7 cells. The gene expression levels of p16INK4a, p21, p27, CHOP, IL-6, IL-8, PAI-1, PTEN and RB1 in MCF-7 cells treated with olaparib for 96 h were significantly up-regulated (P < 0.01) , and the gene expression levels of Ki67 and E2F1 were significantly down-regulated (P < 0.01) . The expression levels of p21, γH2AX and IGFBP3 proteins in MCF-7 cells were significantly increased (P < 0.01, P < 0.01, P < 0.05) , and the expression levels of cyclin D1, pRB and Ki67 proteins were significantly decreased (P < 0.05, P < 0.01, P < 0.05) . Conclusion Olaparib can produce anti-MCF-7 breast cancer cells by anti-proliferation, migration and induction of cell senescence.