Objective This research aimed to: (1) investigate the effects of curcumin in phosphatase and tensin homolog (PTEN)-mediated DNA repair and in the sensitization of wild-type PTEN triple-negative breast cancer cells to Olaparib, a poly ADP ribose polymerase (PARP)1 inhibitor; and (2) provide a new therapeutic strategy for patients with wild-type PTEN triple-negative breast cancer in the clinical setting. Methods Wild-type PTEN and PTEN-deficient variants of the triple-negative breast cancer cell line BT549 were used. MTT was used to assay the cell survival rate. Western blot was performed to detect the expression of RAD51 (a key protein in homologous recombination repair) in wild- type PTEN cells. The comet assay was used to measure the DNA damage caused by curcumin and olaparib. Western blot was used to detect RAD51 after curcumin treatment. Results Wild-type PTEN cells were less sensitive to olaparib than PTEN-deficient BT549 cells. PTEN promoted DNA repair by increasing the expression of RAD51. Curcumin inhibited PTEN-mediated DNA repair by inhibiting RAD51 and enhanced the sensitivity of wild-type PTEN triple-negative breast cancer cells to olaparib. Conclusions Curcumin inhibited PTEN-mediated DNA repair and sensitized wild-type PTEN breast cancer cells to olaparib.