Then, we carried out in vivo and ex vivo experiments to validate the results, and further found that DHIE could inhibit PLK1 in different subtypes of breast cancer, and then regulate the expression of p53 (specifically, downregulate the expression of p53 in triple-negative breast cancer mutant type or upregulate the expression of p53 in wild-type of HER2-overexpressing breast cancer), which resulted in the outcome of the cell-cycle blockade in breast cancer. The gene discussed is PLK1; the disease is triple-negative breast carcinoma.