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

Abstract

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. MTT, flow cytometry, quantitative real-time PCR (qRT-PCR) and western blot assays were performed. 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. The effect of lutein antiproliferation was mediated by activation of the NrF2/ARE pathway, and blocking of the NF-κB signaling pathway.