title: Analysis of the contribution of nasopharyngeal epithelial cancer cells to the induction of a local inflammatory response.
abstract: OBJECTIVE
  We investigated the local contribution of nasopharyngeal epithelial cancer cells to the inflammatory process.
  
  
  METHODS
  THP-1 monocytes were treated with phorbol 12-myristate 13-acetate to induce the production of differentiated macrophages (D-THP-1), which were subsequently activated by lipopolysaccharide (LPS) (10 ng/ml). The production of pro-inflammatory cytokines in D-THP-1 cells was detected by ELISA and qRT-PCR. The effects of conditioned media harvested from LPS-treated D-THP-1 cells were investigated with regard to cell proliferation (MTT), production of pro-inflammatory cytokines (ELISA) and activation of NF-κB and STAT3 (western blot) in the nasopharyngeal epithelial cancer cell line 5-8F.
  
  
  RESULTS
  LPS induced the production of the pro-inflammatory cytokines TNF-α (875.1 ± 68.31 pg/ml), IL-6 (42.2 ± 5.32 pg/ml), IL-1β (9.6 ± 1.34 pg/ml) and IL-8 (19.3 ± 3.47 pg/ml) in D-THP-1 cells significantly (P < 0.001) with similar results detected at the mRNA level. Exposure of 5-8F cells to conditioned medium from LPS-treated D-THP-1 cells significantly induced production of TNF-α (632.3 ± 71.32 pg/ml), IL-6 (51.3 ± 3.57 pg/ml), IL-1β (7.3 ± 1.31 pg/ml) and IL-8 (20.1 ± 2.36 pg/ml) (P < 0.01) and triggered significant activation of NF-κB and STAT3, which correlated with a concomitant degradation of IκBα and an increase in JAK2 phosphorylation (P < 0.05). Moreover, the LPS-treated D-THP-1 conditioned media promoted the proliferation of 5-8F cells (P < 0.05).
  
  
  CONCLUSIONS
  Nasopharyngeal epithelial cancer cells may play a significant role in maintaining and amplifying the inflammation process via activation of NF-κB and STAT3 pathway and through the local production of pro-inflammatory cytokines, which recruit and activate additional immune cells in the nasopharyngeal path and promote tumour progression.
authors.affiliation: Cancer Research Institute, Central South University, 110 Xiang-Ya Road, Changsha, 410078, Hunan, People's Republic of China.
authors.forename: Qianjin
authors.initials: Q
authors.lastname: Liao
authors.forename: Xiaofang
authors.initials: X
authors.lastname: Guo
authors.forename: Xiaoling
authors.initials: X
authors.lastname: Li
authors.forename: Xiayu
authors.initials: X
authors.lastname: Li
authors.forename: Pan
authors.initials: P
authors.lastname: Chen
authors.forename: Fang
authors.initials: F
authors.lastname: Liang
authors.forename: Hailin
authors.initials: H
authors.lastname: Tang
authors.forename: Min
authors.initials: M
authors.lastname: Deng
authors.forename: Minghua
authors.initials: M
authors.lastname: Wu
authors.forename: Jian
authors.initials: J
authors.lastname: Ma
authors.forename: Wei
authors.initials: W
authors.lastname: Xiong
authors.forename: Guiyuan
authors.initials: G
authors.lastname: Li
mesh_terms: D048708:Cell Growth Processes / Q000276:immunology; D002460:Cell Line; D017077:Culture Media, Conditioned; D016207:Cytokines / Q000096:biosynthesis / Q000276:immunology; D004847:Epithelial Cells / Q000276:immunology / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology*; D008070:Lipopolysaccharides / Q000276:immunology / Q000494:pharmacology; D016328:NF-kappa B / Q000276:immunology / Q000378:metabolism; D009303:Nasopharyngeal Neoplasms / Q000276:immunology / Q000473:pathology*; D050796:STAT3 Transcription Factor / Q000276:immunology / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D017077:Culture Media, Conditioned; D016207:Cytokines; D008070:Lipopolysaccharides; D016328:NF-kappa B; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human