Dehydrocorydaline (DHC) is an alkaloid isolated fromCorydali syanhusuothat exhibits antitumor properties. It has been reported that DHC can inhibit the proliferation of breast cancer cells, however the underlying molecular mechanism remains elusive. Therefore, the main objective of this study was to evaluate the antitumor activity of DHC, and gain further insights into its mechanism of action. The viability of MDA-MB-231 cells was determined through a Cell Counting Kit-8 assay. The effect of DHC on the proliferation of MDA-MB-231 cells was detected by flow cytometry and 5-ethynyl-2 '-deoxyuridine staining. Apoptosis was evaluated by Annexin V-FITC and PI staining through flow cytometry. The impact of DHC treatment on the colony-forming ability of breast cancer cells was assessed. The expression levels of proliferation-associated genes cyclin-dependent kinases 1 (CDK1) and cyclin D1 (CCND1) and apoptosis-related genesBCL2andcaspases 3/8/9were quantified by real-time PCR. Western blot analysis was performed to evaluate the production of cleaved caspase 3/9 and matrix metalloproteinase (MMP)2/9. DHC-treated MDA-MB-231 cells were subcutaneously injected into mice. Subsequent immunohistochemical analyses were performed. DHC inhibited the viability, proliferation, colony-forming ability and migration of MDA-MB-231 cells; in addition, DHC treatment promoted their apoptosis. DHC inhibited the production of proliferation- and anti-apoptosis-associated proteins CDK1, CCND1, BCL2 as well as that of the metastasis-associated proteins MMP2 and MMP9. However, it promoted the expression of the pro-apoptotic caspases 3/8/9. Moreover, DHC inhibited the growth of MDA-MB-231 tumor xenografts in SCID mice, and decreased cell proliferation in newly formed tumorsin vivo. DHC exerted anticancer effects by downregulating cell proliferation, antiapoptosis, metastasis-associated proteins CDK1, CCND1, BCL2 and metastasis-associated proteins MMP2 and MMP9, and by upregulating the expression of proapoptotic proteins caspase 3/8/9.