Poly(I:C) potentiates Bacillus Calmette-Guérin immunotherapy for bladder cancer

Cancer Immunol Immunother. 2016 Feb;65(2):223-34. doi: 10.1007/s00262-015-1789-y. Epub 2016 Jan 12.

Abstract

Non-specific immunotherapy consisting of intravesical instillation of Bacillus Calmette-Guérin (BCG) is currently the best available treatment to prevent non-muscle-invasive bladder tumor recurrence and progression. This treatment however is suboptimal, and more effective immunotherapeutic approaches are needed. Toll-like receptors (TLRs) play a major role in the activation of the immune system in response to pathogens and danger signals but also in anti-tumor responses. We previously showed that human urothelial cells express functional TLRs and respond to TLR2 and TLR3 agonists. In this study, we analyzed the potential of polyinosinic:polycytidylic acid [poly(I:C)], a TLR3 agonist, to replace or complement BCG in the treatment of non-muscle-invasive bladder cancer. We observed that poly(I:C) had an anti-proliferative, cytotoxic, and apoptotic effect in vitro on two low-grade human bladder cancer cell lines, MGH-U3 and RT4. In MGH-U3 cells, poly(I:C) induced growth arrest at the G1-S transition. Poly(I:C) also increased the immunogenicity of MGH-U3 and RT4 cells, inducing the secretion of MHC class I molecules and of pro-inflammatory cytokines. By comparison, poly(I:C) had less in vitro impact on two high-grade human bladder cancer cell lines, 5637 and T24, and on MBT-2 murine high-grade bladder cancer cells. The latter can be used as an immunocompetent model of bladder cancer. The combination poly(I:C)/BCG was much more effective in reducing MBT-2 tumor growth in mice than either treatment alone. It completely cured 29% of mice and also induced an immunological memory response. In conclusion, our study suggests that adding poly(I:C) to BCG may enhance the therapeutic effect of BCG.

Keywords: BCG; Bladder cancer; Immunotherapy; Mouse model; Poly(I:C); TLR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Cell Cycle Checkpoints / drug effects
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cytokines / metabolism
  • Disease Models, Animal
  • Gene Expression
  • Histocompatibility Antigens Class I / genetics
  • Histocompatibility Antigens Class I / immunology
  • Humans
  • Immunotherapy* / methods
  • Inflammation Mediators / metabolism
  • Mice
  • Mycobacterium bovis / immunology*
  • Poly I-C / immunology*
  • Poly I-C / pharmacology
  • Tumor Burden / drug effects
  • Tumor Burden / immunology
  • Urinary Bladder Neoplasms / genetics
  • Urinary Bladder Neoplasms / immunology*
  • Urinary Bladder Neoplasms / metabolism
  • Urinary Bladder Neoplasms / mortality
  • Urinary Bladder Neoplasms / pathology*
  • Urinary Bladder Neoplasms / therapy
  • Xenograft Model Antitumor Assays

Substances

  • Cytokines
  • Histocompatibility Antigens Class I
  • Inflammation Mediators
  • Poly I-C