NrF2/ARE and NF-κB pathway regulation may be the mechanism for lutein inhibition of human breast cancer cell. (April 2018)

• Record Type: Journal Article
• Authors: Chang, Jingzhi; Zhang, Yuxia; Li, Yichuan; Lu, Kun; Shen, Yongjie; Guo, Yali; Qi, Qingfeng; Wang, Mingchen; Zhang, Shanfeng
• Is Part Of: Future oncology. Volume 14:Number 8(2018)
• Page Start: 719
• Page End: 726
• Publication Date: 2018-04
• Subjects: breast cancer -- lutein -- NF-κB signaling pathway -- NrF2/ARE signaling pathway -- proliferation; Oncology -- Periodicals; 616.99405
• DOI: 10.2217/fon-2017-0584
• Languages: English
• ISSNs: 1479-6694

Abstract

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.