title: [Inflammatory factors promote oral squamous cell carcinoma cells metastasis, via nuclear factor kappa B signal pathway in vitro].
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.
authors.affiliation: Department of Oral and Maxillofacial Surgery, Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine & Shanghai Research Institute of Stomatology & Shanghai Key Laboratory of Stomatology, Shanghai 200011, China.
authors.forename: Ming
authors.initials: M
authors.lastname: Yan
authors.forename: Di
authors.initials: D
authors.lastname: He
authors.forename: Ping
authors.initials: P
authors.lastname: Zhang
authors.forename: Xiao-Jian
authors.initials: XJ
authors.lastname: Zhou
authors.forename: Wan-Tao
authors.initials: WT
authors.lastname: Chen
mesh_terms: D002294:Carcinoma, Squamous Cell / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D002465:Cell Movement; D016207:Cytokines / Q000378:metabolism*; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000378:metabolism; D006801:Humans; D020672:I-kappa B Proteins / Q000378:metabolism; D053582:Interleukin-1alpha / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism*; D010766:Phosphorylation; D011392:Proline / Q000031:analogs & derivatives / Q000494:pharmacology; D015398:Signal Transduction; D013859:Thiocarbamates / Q000494:pharmacology; D014062:Tongue Neoplasms / Q000378:metabolism / Q000473:pathology; D051996:Transcription Factor RelA / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D020672:I-kappa B Proteins; D053582:Interleukin-1alpha; D015850:Interleukin-6; D016209:Interleukin-8; D016328:NF-kappa B; C000606204:NFKBIA protein, human; D013859:Thiocarbamates; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; C066229:prolinedithiocarbamate; D000072000:NF-KappaB Inhibitor alpha; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D011392:Proline