Sulforaphane inhibits metastatic potential of human breast cancer cells by modulating EMT markers and Wnt/β-catenin signaling pathway

Introduction & Aim: Metastasis is the primary cause of death in the majority of breast cancer patients that are not sensitive to radiotherapy or chemotherapy. Epithelial-mesenchymal transition (EMT) plays an important role in breast cancer metastasis. The aberrant activation of Wnt/β-catenin pathway, a key regulator of normal tissue development, contributes to the process of EMT. Thus, targeting the EMT inducers represents an important therapeutic strategy for preventing or treating breast cancer metastasis. Natural products due to less side effects and therapeutic activities constitute a common alternative for conventional treatments. Sulforaphane (SFN), a compound derived from cruciferous plants, exhibits anti-metastatic properties. Here we investigated the molecular mechanism by which SFN suppressed tumor metastasis in relation with EMT and β-catenin expression. Methods: MDA-MB-231 cells were treated with different concentrations of SFN. After 24, 48 and 72 hours, inhibitory effect of SFN on cell migration was evaluated by scratch and transwell migration assay and induction of apoptosis was assessed by flow cytometry analysis. Then, the effect of SFN on expression levels of ZEB 1, claudin and β-catenin as key regulators of EMT were evaluated. Results: Our results indicated that SFN induced cell apoptosis and significantly retarded the migration of MDA-MB-231 cells. Moreover SFN, reduced the expression of ZEB1, claudin and β-catenin in MDA-MB-231 cells. Conclusion: SFN inhibited the metastatic ability of breast cancer cells by suppressing the expression of EMT associated genes and β-catenin. SFN might be a potential therapeutic agent in combination with other anticancer drugs.