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Blocking transforming growth factor-β signaling pathway augments antitumor effect of adoptive NK-92 cell therapy

Int Immunopharmacol. 2013 Oct;17(2):198-204. doi: 10.1016/j.intimp.2013.06.003. Epub 2013 Jun 25.

Abstract

Natural killer (NK) cells hold great potential for improving the immunotherapy of cancer. However, existing data indicate that tumor cells can effectively escape NK cell-mediated apoptosis through immunosuppressive effect in the tumor microenvironment. Transforming growth factor-β (TGF-β) is a potent immunosuppressant. The present study was intended to develop a treatment strategy through adoptive transfer of TGF-β insensitive NK-92 cells. To block TGF-β signaling pathway, NK-92 cells were genetically modified with dominant negative TGF-β type II receptor (DNTβRII) by optimizing electroporation using the Amaxa Nucleofector system. These genetically modified NK-92 cells were insensitive to TGF-β and able to resist the suppressive effect of TGF-β on Calu-6 lung cancer cells in vitro. To determine the antitumor activity in vivo, recipient mice were challenged with a single subcutaneous injection of Calu-6 cells. Adoptive transfer of TGF-β insensitive NK-92 cells decreased tumor proliferation, reduced lung metastasis, produced more IFN-γ, and increased the survival rate of nude mice bearing established Calu-6 cells. Hence, we have demonstrated that blocking transforming growth factor-β signaling pathway in NK cells provides a novel therapeutic strategy and warrants further investigation.

Keywords: Adoptive cell therapy; Cancer; Natural killer-92 cell; Nucleofection; Transforming growth factor-β.

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Cytotoxicity, Immunologic
  • Humans
  • Immunosuppression Therapy
  • Immunotherapy, Adoptive / methods*
  • Killer Cells, Natural / immunology*
  • Killer Cells, Natural / transplantation
  • Lung Neoplasms / immunology
  • Lung Neoplasms / therapy*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Neoplasms, Experimental / immunology
  • Neoplasms, Experimental / therapy*
  • Phosphorylation
  • Protein Serine-Threonine Kinases / antagonists & inhibitors*
  • Receptor, Transforming Growth Factor-beta Type II
  • Receptors, Transforming Growth Factor beta / antagonists & inhibitors*
  • Signal Transduction
  • Smad2 Protein / metabolism
  • Transforming Growth Factor beta / antagonists & inhibitors*
  • Transgenes / genetics
  • Tumor Microenvironment
  • Xenograft Model Antitumor Assays

Substances

  • Receptors, Transforming Growth Factor beta
  • Smad2 Protein
  • Transforming Growth Factor beta
  • Protein Serine-Threonine Kinases
  • Receptor, Transforming Growth Factor-beta Type II