TLR3 Expression Induces Apoptosis in Human Non-Small-Cell Lung Cancer.

Francesca Bianchi, Spyridon Alexiadis, Chiara Camisaschi, Mauro Truini, Giovanni Centonze, Massimo Milione, Andrea Balsari, Elda Tagliabue, Lucia Sfondrini

Research output: Contribution to journalArticlepeer-review


The prognostic value of Toll-like receptor 3 (TLR3) is debated in cancer, differing between tumor types, methods, and cell types. We recently showed for the first time that TLR3 expression on early stage non-small-cell lung cancer (NSCLC) results associated with a good prognosis. Here, we provide experimental evidences explaining the molecular reason behind TLR3's favorable prognostic role. We demonstrated that TLR3 activation in vitro induces apoptosis in lung cancer cell lines and, accordingly, that TLR3 expression is associated with caspase-3 activation in adenocarcinoma NSCLC specimens, both evaluated by immunohistochemistry. Moreover, we showed that TLR3 expression on cancer cells contributes to activate the CD103+ lung dendritic cell subset, that is specifically associated with processing of antigens derived from apoptotic cells and their presentation to CD8+ T lymphocytes. These findings point to the relevant role of TLR3 expression on lung cancer cells and support the use of TLR3 agonists in NSCLC patients to re-activate local innate immune response.
Original languageEnglish
JournalInternational Journal of Molecular Sciences
Issue number4
Publication statusPublished - Feb 1 2020


  • Humans
  • dendritic cells
  • apoptosis
  • Cell Line
  • Tumor
  • Immunotherapy
  • Animals
  • Mice
  • CD103
  • IHC
  • poly(I:C)
  • toll-like receptor 3 (TLR3)
  • Apoptosis/*immunology
  • Carcinoma
  • Non-Small-Cell Lung/*immunology/pathology/therapy
  • Caspase 3/immunology
  • Gene Expression Regulation
  • Neoplastic/*immunology
  • Immunity
  • Innate
  • Lung Neoplasms/*immunology/pathology/therapy
  • Neoplasm Proteins/*immunology
  • Toll-Like Receptor 3/agonists/*immunology


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