Breast cancer (BC) is one of the most common malignant
tumors found in females. Previous studies have demonstrated that
curcumin, which is a type of
polyphenol compound extracted from Curcuma longa underground rhizome, is able to inhibit the survival of
cancer cells. However, the functional role and mechanism of
curcumin in BC are still unclear. The Cell Counting Kit-8 assay was performed to examine the effects of
curcumin on cell viability in the BC cell lines MDA-MB-453 and MCF-7. The levels of
lipid reactive oxygen species (ROS),
malondialdehyde (MDA) production, and intracellular Fe2+ were determined to assess the effects of
curcumin on cell ferroptosis. Western blot analysis was also carried out to detect the
protein levels. Finally, the antitumorigenic effect of
curcumin on BC was identified in a xenograft
tumor model. In the present study, the results indicated that
curcumin could dose-dependently suppress the viability of both MDA-MB-453 and MCF-7 cells. Further studies revealed that
curcumin facilitated solute carrier family 1 member 5 (SLC1A5)-mediated ferroptosis in both MDA-MB-453 and MCF-7 cells by enhancing
lipid ROS levels, lipid peroxidation end-product MDA accumulation, and intracellular Fe2+ levels. In vivo experiments demonstrated that
curcumin could significantly hamper
tumor growth. Collectively, the results demonstrated that
curcumin exhibited antitumorigenic activity in BC by promoting SLC1A5-mediated ferroptosis, which suggests its use as a potential therapeutic agent for the treatment of BC.