Targeting Tumorigenicity of Breast Cancer Stem Cells Using SAHA/Wnt-b Catenin Antagonist Loaded Onto Protein Corona of Gold Nanoparticles

Int J Nanomedicine. 2020 Jun 11:15:4063-4078. doi: 10.2147/IJN.S234636. eCollection 2020.

Abstract

Background: Among various theories for the origin of cancer, the "stemness phenotype model" suggests a dynamic feature for tumor cells in which non-cancer stem cells (non-CSCs) can inter-convert to CSCs. Differentiation with histone-deacetylase inhibitor, vorinostat (SAHA), can induce stem cells to differentiate as well as enforces non-CSCs to reprogram to CSCs. To avoid this undesirable effect, one can block the Wnt-βcatenin pathway. Thus, a dual delivery system of SAHA and a Wnt-βcatenin blocker will be beneficial in the induction of differentiation of CSCs. Protein corona (PC) formation in nanoparticle has a biologic milieu, and despite all problematic properties, it can be employed as a medium for dual loading of the drugs.

Materials and methods: We prepared sphere gold nanoparticles (GNPs) with human plasma protein corona loaded with SAHA as differentiating agent and PKF118-310 (PKF) as a Wnt-βcatenin antagonist. The MCF7 breast cancer stem cells were treated with NPs and the viability and differentiation were evaluated by Western blotting and sphere formation assay.

Results: We found that both drugs loaded onto corona-capped GNPs had significant cytotoxicity in comparison to bare GNP-corona. Data demonstrated an increase in stem cell population and upregulation of mesenchymal marker, Snail by SAHA-loaded GNPs treatment; however, the combination of PKF loaded GNPs along with SAHA-loaded GNPs resulted in a reduction of stem cell populations and Snail marker. We have shown that in MCF7 and its CSCs simultaneous treatment with SAHA and PKF118-310 induced differentiation and inhibition of Snail induction.

Conclusion: Our study reveals the PC-coated GNPs as a biocompatible career for both hydrophilic (PKF) and hydrophobic (SAHA) agents which can decrease breast cancer stem cell populations along with reduced stemness state regression.

Keywords: HDAC inhibitor; Wnt; cancer stem cell; co-delivery; protein corona.

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects
  • Breast Neoplasms / pathology*
  • Carcinogenesis / drug effects
  • Carcinogenesis / pathology*
  • Cell Survival / drug effects
  • Drug Liberation
  • Endocytosis / drug effects
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects
  • Gold / chemistry*
  • Histone Deacetylase Inhibitors / pharmacology
  • Humans
  • MCF-7 Cells
  • Metal Nanoparticles / chemistry*
  • Nanospheres / chemistry
  • Neoplastic Stem Cells / drug effects
  • Neoplastic Stem Cells / pathology*
  • Protein Corona / chemistry*
  • Spectrophotometry, Ultraviolet
  • Vorinostat / pharmacology*
  • Wnt Proteins / antagonists & inhibitors*
  • Wnt Proteins / metabolism
  • beta Catenin / antagonists & inhibitors
  • beta Catenin / metabolism

Substances

  • Antineoplastic Agents
  • Histone Deacetylase Inhibitors
  • Protein Corona
  • Wnt Proteins
  • beta Catenin
  • Vorinostat
  • Gold