Quercetin induces apoptosis and necroptosis in MCF-7 breast cancer cells

Bratisl Lek Listy. 2017;118(2):123-128. doi: 10.4149/BLL_2017_025.

Abstract

Objective: This study investigated the quercetin (Que) effects on growth of MCF-7 human cancer breast cell line and its cellular death mechanism.

Background: Quercetin has been found to be very efficacious against many different types of cancer cells. However, the study is not sufficiently powered to demonastrate anticancer mechanisms.

Methods: MCF-7cells were treated by 50 µM/ ml of Que for 48 hours. MCF-7 cells were also pretreated with 10 Μm ZVAD (apoptosis inhibitor) or 3 mM Nec-1 (necroptosis inhibitor) for evaluation of cell death induced by apoptosis or necroptosis.

Results: MTT and clonogenicity assays revealed that the Que induced a significant increase in cell viability and proliferation in presence of Nec-1 in comparison to the presence of ZVAD (p < 0.05). Que also increased apoptosis as revealed by DAPI staining and morphology evaluations. Following Que treatment Bcl-2 expression was significantly decreased while Bax expression was significantly increased. Que in presence of Nec-1 decreased expression of Bax gene, reduced apoptotic index, increased cell viability and proliferation of MCF-7 cells in comparison to absence of Nec-1. MCF-7 cells showed a significantly increased expression of RIPK1 and RIPK3 in response to Que plus ZVAD in comparison to absence of ZVAD.

Conclusion: Our results revealed that the high Que toxicity for breast cancer cells depends on multiple cell death pathways, which involve mainly necroptosis (Fig. 6, Ref. 21).

Keywords: apoptosis; necroptosis; quercetin breast cancer..

MeSH terms

  • Antioxidants / pharmacology*
  • Apoptosis / drug effects*
  • Breast Neoplasms / metabolism
  • Cell Death
  • Cell Survival / drug effects
  • Female
  • Humans
  • MCF-7 Cells / drug effects*
  • Necrosis / drug therapy*
  • Quercetin / metabolism
  • Quercetin / pharmacology*
  • Receptor-Interacting Protein Serine-Threonine Kinases

Substances

  • Antioxidants
  • Quercetin
  • RIPK1 protein, human
  • RIPK3 protein, human
  • Receptor-Interacting Protein Serine-Threonine Kinases