Objective: Despite the rapidly developing diagnosis and treatment strategies in recent years, breast cancer is the most common type of cancer in women and is the cause of cancer-related death. Embelin is a potent XIAP inhibitor and a compound with antiestrogenic effects. In our study, we aimed to investigate the antitumoral activities of Embelin, which shows its effects through different cellular pathways, in two different human breast cancer cell lines, hormone receptor negative (MDA-MB-231) and positive (MCF-7) and we compared the effects of Embelin with tamoxifen and docetaxel, which are currently widely used in the treatment of breast cancer. Methods: To demonstrate the effects of Embelin at the cellular level, cytotoxicity analyzes and IC50 calculations were performed with a real-time cell electronic detection system (xCELLigence). For all subsequent studies, cells were treated with the IC50 dose of Embelin which determined in cytotoxicity assays and histopathological and immunohistochemical (Ki-67, Bax, Bcl-2, Cyclin D1) analyzes were performed. Results: As a result of cell cytotoxicity analyzes, it was observed that Embelin had an antiproliferative effect in both cancer cell types in a dose and time dependent manner. IC50 values were calculated as 63 pM for MCF-7 and 64 pM for MDA-MB-231 from the proliferation curve graphs of Embelin exposed cells. As a result of the examination of the preparations stained with Hematoksylin-Eosin (H&E) and Ki-67, it was found that the cell number and Ki-67 proliferation index decreased (p<0.05) in cancer cells treated with Embelin. In order to analyze the effects of Embelin on the cell cycle, when we examined the preparations stained with Cyclin D1, it was observed that embelin decreased the Cyclin D1 levels required for the S1 phase of the cell cycle (p<0.05). In order to see the effect of Embelin on apoptotic pathways, preparations stained with proapoptotic Bax and antiapoptotic Bcl-2 were examined. Accordingly, while Bax expression level increased (p<0.05), Bcl-2 expression level decreased (p<0.05). Conclusion: In general, Embelin inhibits cancer cell proliferation in both breast cancer cell types, depending on dose and time. We found that Embelin was statistically more effective at the molecular level when compared to both Tamoxifen and Docetaxel, especially in hormone receptor-negative MDA MB-231 cells. By concluding that it is more effective especially in hormone receptor-negative breast cancer, Embelin may be an alternative new antitumoral agent in the treatment of breast cancer in the future. The results of this study may guide for in vivo studies in future.