Cancers Cells in Traps? The Pathways of NETs Formation in Response to OSCC in Humans-A Pilot Study

Cancer Control. 2020 Jan-Dec;27(1):1073274820960473. doi: 10.1177/1073274820960473.

Abstract

The aim of the experiment was to evaluate the process of neutrophil extracellular traps (NETs) formation in patients with oral squamous cell carcinoma (OSCC) in response to direct or indirect contact with SCC cells in comparison to results obtained in the cells of healthy subjects. To fulfill study objectives CAL 27 cell line and blood were obtained from cancer patients and control subjects. Parameters related to NETs formation were analyzed utilizing flow cytometry, fluorescence microscopy, and ELISA-type tests. The expression of selected phosphorylated proteins of the PI3K/Akt/PBK pathway in neutrophils was evaluated using the Western blot method. An increase in NETs formation was observed in a coculture of neutrophils with SCC cells, with the largest amount of NETs formed after stimulation with a supernatant obtained from the SCC culture. The enhanced process of NETs formation was accompanied by changes in the expression of proteins from the PI3K/Akt/PBK pathway. The obtained results prove the existence of interactions between neutrophils and cancer cells resulting in NETosis with the participation of the PI3K/Akt/PBK pathway in patients with OSCC.

Keywords: NETs; PI3K/Akt/PBK; SCC; neutrophils; oral cancer.

MeSH terms

  • Adult
  • Aged
  • Case-Control Studies
  • Cell Line, Tumor
  • Class I Phosphatidylinositol 3-Kinases / metabolism
  • Coculture Techniques
  • Extracellular Traps*
  • Female
  • Head and Neck Neoplasms / metabolism
  • Head and Neck Neoplasms / pathology*
  • Humans
  • Male
  • Middle Aged
  • Pilot Projects
  • Proto-Oncogene Proteins c-akt / metabolism
  • Squamous Cell Carcinoma of Head and Neck / metabolism
  • Squamous Cell Carcinoma of Head and Neck / pathology*

Substances

  • Class I Phosphatidylinositol 3-Kinases
  • PIK3CA protein, human
  • AKT1 protein, human
  • Proto-Oncogene Proteins c-akt