Inhibition of Bone Marrow-Derived Mesenchymal Stem Cells Homing Towards Triple-Negative Breast Cancer Microenvironment Using an Anti-PDGFRβ Aptamer

Theranostics. 2017 Aug 22;7(14):3595-3607. doi: 10.7150/thno.18974. eCollection 2017.

Abstract

Bone marrow-derived mesenchymal stem cells (BM-MSCs) are shown to participate in tumor progression by establishing a favorable tumor microenvironment (TME) that promote metastasis through a cytokine networks. However, the mechanism of homing and recruitment of BM-MSCs into tumors and their potential role in malignant tissue progression is poorly understood and controversial. Here we show that BM-MSCs increase aggressiveness of triple-negative breast cancer (TNBC) cell lines evaluated as capability to migrate, invade and acquire stemness markers. Importantly, we demonstrate that the treatment of BM-MSCs with a nuclease-resistant RNA aptamer against platelet-derived growth factor receptor β (PDGFRβ) causes the inhibition of receptor-dependent signaling pathways thus drastically hampering BM-MSC recruitment towards TNBC cell lines and BM-MSCs trans-differentiation into carcinoma-associated fibroblast (CAF)-like cells. Moreover, in vivo molecular imaging analysis demonstrated the aptamer ability to prevent BM-MSCs homing to TNBC xenografts. Collectively, our results indicate the anti-PDGFRβ aptamer as a novel therapeutic tool to interfere with BM-MSCs attraction to TNBC providing the rationale to further explore the aptamer in more complex pre-clinical settings.

Keywords: Bone marrow-derived mesenchymal stem cells; aptamer; platelet-derived growth factor receptor β; triple-negative breast cancer..

MeSH terms

  • Animals
  • Aptamers, Nucleotide / genetics*
  • Cell Movement*
  • Cell Transdifferentiation
  • Cells, Cultured
  • Female
  • Fibroblasts / metabolism
  • Fibroblasts / pathology
  • Humans
  • MCF-7 Cells
  • Mesenchymal Stem Cells / metabolism*
  • Mesenchymal Stem Cells / pathology
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • RNAi Therapeutics / methods
  • Receptor, Platelet-Derived Growth Factor beta / genetics*
  • Receptor, Platelet-Derived Growth Factor beta / metabolism
  • Triple Negative Breast Neoplasms / metabolism
  • Triple Negative Breast Neoplasms / pathology
  • Triple Negative Breast Neoplasms / therapy*
  • Tumor Microenvironment*

Substances

  • Aptamers, Nucleotide
  • Receptor, Platelet-Derived Growth Factor beta