NrF2/ARE and NF-κB pathway regulation may be the mechanism for lutein inhibition of human breast cancer cell.

AIM: Though lutein can inhibit cancer cell proliferation via alleviating oxidative injury, the molecular mechanisms of lutein involvement in the NrF2/antioxidant response element (ARE) and NF-κB pathways remain poorly understood.

MATERIALS & METHODS: MTT, flow cytometry, quantitative real-time PCR (qRT-PCR) and western blot assays were performed.

RESULTS: After treatment with lutein, breast cancer cell proliferation was significantly decreased in a dose-dependent manner. Lutein induced nuclear translocation and protein expression of NrF2, improved the expression of cellular antioxidant enzymes and attenuated reactive oxygen species levels. Moreover, lutein treatment decreased NF-κB signaling pathway related NF-κB p65 protein expression.

CONCLUSION: The effect of lutein antiproliferation was mediated by activation of the NrF2/ARE pathway, and blocking of the NF-κB signaling pathway.