[Inflammatory factors promote oral squamous cell carcinoma cells metastasis, via nuclear factor kappa B signal pathway in vitro]

Zhonghua Kou Qiang Yi Xue Za Zhi. 2010 Mar;45(3):146-51.
[Article in Chinese]

Abstract

Objective: To investigate the roles of inflammatory factors and nuclear factor kappa B (NF-kappaB) signal pathway in metastasis of oral squamous cell carcinoma.

Methods: The oral squamous cell carcinoma cell lines with highly metastasis potential (Tb) and lower metastasis potential (Tca8113) were used in this study. The levels of NF-kappaB activity in oral squamous cell carcinoma cell lines were determined by Western blotting and luciferase reporter assay. pBalphabe-IkappaBalpha-SR expression vector or NF-kappaB inhibitor pyrolidinedithiocarbamate (PDTC) was used to inhibit NF-kappaB, and cell migration was examined by transwell assay. The secretion of tumor necrosis factor-alpha (TNF-alpha), IL-1alpha, IL-6, IL-8 and GM-CSF proinflammatory cytokines was determined by ELISA when Tb cells were transfected with pBalphabe-SR-IkappaBalpha or treated with PDTC.

Results: Western blotting showed that the levels of phosphorIkappaBalpha and phosphor-p65 were highly expressed in Tb cells. Tb cells had high level of constitutive NF-kappaB activity and were more sensitive to TNF-alpha. The migration of highly metastatic Tb cells, either transfected with dominant-negative mutant inhibitor pBalphabe-SR-IkappaBalpha or treated with PDTC, was suppressed when determined by transwell assay. The secretion of proinflammatory cytokines, including TNF-alpha, IL-1alpha, IL-6, IL-8 and granulocyte-macrophage colony stimulating factor (GM-CSF), was inhibited by pBalphabe-SR-IkappaBalpha transfection or PDTC treatment.

Conclusions: The inflammatory factors such as TNF-alpha could promote oral squamous cell carcinoma cell metastasis via NF-kappaB signal pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Squamous Cell* / metabolism
  • Carcinoma, Squamous Cell* / pathology
  • Cell Line, Tumor
  • Cell Movement*
  • Cytokines / metabolism*
  • Granulocyte-Macrophage Colony-Stimulating Factor / metabolism
  • Humans
  • I-kappa B Proteins / metabolism
  • Interleukin-1alpha / metabolism
  • Interleukin-6 / metabolism
  • Interleukin-8 / metabolism
  • NF-KappaB Inhibitor alpha
  • NF-kappa B / metabolism*
  • Phosphorylation
  • Proline / analogs & derivatives
  • Proline / pharmacology
  • Signal Transduction
  • Thiocarbamates / pharmacology
  • Tongue Neoplasms* / metabolism
  • Tongue Neoplasms* / pathology
  • Transcription Factor RelA / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Cytokines
  • I-kappa B Proteins
  • Interleukin-1alpha
  • Interleukin-6
  • Interleukin-8
  • NF-kappa B
  • NFKBIA protein, human
  • Thiocarbamates
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • prolinedithiocarbamate
  • NF-KappaB Inhibitor alpha
  • Granulocyte-Macrophage Colony-Stimulating Factor
  • Proline