Fullerenol inhibits the cross-talk between bone marrow-derived mesenchymal stem cells and tumor cells by regulating MAPK signaling

Xin Nie, Jinglong Tang, Ying Liu, Rong Cai, Qing Miao, Yuliang Zhao, Chunying Chen

Research output: Contribution to journalArticle

11 Scopus citations

Abstract

The interaction between bone marrow-derived mesenchymal stem cells (BDMSCs) and tumor cells promotes tumor proliferation and metastasis. We found that 4T1 breast cancer cells induced malignant differentiation of BDMSCs and that BDMSCs also affected the growth and metastasis of 4T1 cells. However, when the interaction between BDMSCs and 4T1 cells was attenuated or blocked by C60(OH)22 nanoparticles, tumor growth and metastasis were significantly suppressed. The suppression of metastasis depended on the activation of MAPK signals in the BDMSCs, whereas the underlying pathways were related to a broad range of extracellular responses and were modulated by the secretion of multiple cytokines. Interestingly, C60(OH)22 regulated the malignantly differentiated BDMSCs via the Erk- and p38-MAPK and its downstream NF-κB signal pathway, but in normal BDMSCs regulation occurred only through Erk- and p38-MAPK and not by NF-κB activation. This study may provide a novel mechanism for C60(OH)22 nanoparticles as an anti-tumor drug.

Original languageEnglish (US)
Pages (from-to)1879-1890
Number of pages12
JournalNanomedicine: Nanotechnology, Biology, and Medicine
Volume13
Issue number6
DOIs
StatePublished - Aug 2017

Keywords

  • 4T1 tumor cells
  • Bone marrow-derived mesenchymal stem cells
  • Fullerenol
  • MAPK signaling

ASJC Scopus subject areas

  • Bioengineering
  • Medicine (miscellaneous)
  • Molecular Medicine
  • Biomedical Engineering
  • Materials Science(all)
  • Pharmaceutical Science

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