title: Wound-healing factors can prime head and neck cancer cells to increase their tumor-forming capacity.
abstract: We investigated whether exposing a wound-healing-sensitive cell line to human wound fluid (HWF) could prime the cells to increase their tumor-forming ability in nude mice and, if so, whether this ability can be inhibited by pharmacological substances.
  
  
  
  Experimental animal model.
  
  
  
  Take rate was measured in BALB/c nude mice after pretreatment of the cells with HWF using human serum and fetal bovine serum as controls. Inhibition of signal transducer and activator of transcription 3 (STAT3) with S3I-201 tocilizumab, and of interleukin 6 receptor (IL6R) with tocilizumab was performed.
  
  
  
  Preincubation with HWF resulted in a significant increase in take rate compared to controls. The increase in take rate could be decreased by both STAT3 and IL6R inhibition.
  
  
  
  The results indicate that head and neck squamous cell cancer cells might be stimulated to increase their tumor-forming ability both close to a surgical wound and at more distant locations, as a consequence of the wound-healing response. The work also suggests new treatment modalities aimed at decreasing these stimulatory effects.
  
  
  
  NA Laryngoscope, 126:E213-E217, 2016.
authors: Department of Clinical Sciences, Division of Otolaryngology/Head and Neck Surgery, Lund University, Lund, Sweden, Skåne University Hospital, Lund, Sweden.
authors: Gustaf
authors: G
authors: Lindgren
authors: Department of Clinical Sciences, Division of Oncology and Pathology, Lund University, Lund, and Skåne University Hospital, Lund, Sweden.
authors: Elisabeth
authors: E
authors: Kjellén
authors: Department of Clinical Sciences, Division of Otolaryngology/Head and Neck Surgery, Lund University, Lund, Sweden, Skåne University Hospital, Lund, Sweden.
authors: Johan
authors: J
authors: Wennerberg
authors: Department of Clinical Sciences, Division of Oncology and Pathology, Lund University, Lund, and Skåne University Hospital, Lund, Sweden.
authors: Lars
authors: L
authors: Ekblad
mesh_terms: D000636:Aminosalicylic Acids / Q000494:pharmacology; D000818:Animals; D061067:Antibodies, Monoclonal, Humanized / Q000494:pharmacology*; D001557:Benzenesulfonates / Q000494:pharmacology*; D063646:Carcinogenesis / Q000187:drug effects*; D045744:Cell Line, Tumor; D006258:Head and Neck Neoplasms / Q000209:etiology / Q000517:prevention & control*; D006801:Humans; D051379:Mice; D008807:Mice, Inbred BALB C; D019947:Receptors, Interleukin-6 / Q000037:antagonists & inhibitors; D050796:STAT3 Transcription Factor / Q000037:antagonists & inhibitors; D014945:Wound Healing / Q000502:physiology*
chemical_list: D000636:Aminosalicylic Acids; D061067:Antibodies, Monoclonal, Humanized; D001557:Benzenesulfonates; C520337:NSC 74859; D019947:Receptors, Interleukin-6; D050796:STAT3 Transcription Factor; C494087:Stat3 protein, mouse; C502936:tocilizumab
keywords: Head and neck squamous cell carcinoma; interleukin 6 receptor; metastasis; signal transducer and activator of transcription 3; tocilizumab; wound healing