Anticancer Effects of Broccoli Sprout Extract and Sulforaphane Through ROS-Induced MAPK Pathway in Breast Cancer Cells and Xenografts

Breast cancer treatment remains challenging due to therapeutic resistance and the limited availability of effective molecular targets. We investigated the anticancer effects of sulforaphane (SFN) and broccoli sprout extract (BSE), an SFN-enriched phytochemical formulation, in MCF7 and MDA-MB-231 breast cancer cells. Cell viability, colony formation, and apoptotic responses were evaluated using standard in vitro assays, and underlying mechanisms were examined by flow cytometry and Western blot analysis. BSE and SFN reduced cell viability in a dose-dependent manner, suppressed anchorage-independent growth, and induced apoptosis associated with increased reactive oxygen species (ROS) generation and activation of c-Jun N-terminal kinase and p38 MAPK signaling pathways. These effects were accompanied by mitochondrial depolarization, G2/M cell cycle arrest, and caspase activation. Pharmacokinetic analysis in rats demonstrated that oral administration of BSE resulted in sustained, dose-dependent systemic exposure to SFN. Consistent with these findings, oral BSE significantly inhibited tumor growth in breast cancer xenograft models. Collectively, these results indicate that BSE exerts anticancer effects through coordinated modulation of ROS-associated MAPK signaling, mitochondrial dysfunction, and apoptotic pathways, and may serve as a promising orally administered SFN-containing phytochemical formulation that may function as a delivery matrix for breast cancer management.