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

Future Oncol. 2018 Apr;14(8):719-726. doi: 10.2217/fon-2017-0584. Epub 2018 Jan 16.

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.

Keywords: NF-κB signaling pathway; NrF2/ARE signaling pathway; breast cancer; lutein; proliferation.

MeSH terms

  • Antioxidant Response Elements / genetics
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / genetics
  • Breast Neoplasms / pathology
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Lutein / pharmacology*
  • NF-E2-Related Factor 2 / genetics*
  • Oxidative Stress / drug effects
  • Reactive Oxygen Species / metabolism
  • Signal Transduction / drug effects
  • Transcription Factor RelA / genetics*

Substances

  • NF-E2-Related Factor 2
  • NFE2L2 protein, human
  • Reactive Oxygen Species
  • Transcription Factor RelA
  • Lutein