Porphyromonas gingivalis promotes the motility of esophageal squamous cell carcinoma by activating NF-κB signaling pathway

Microbes Infect. 2019 Aug-Sep;21(7):296-304. doi: 10.1016/j.micinf.2019.01.005. Epub 2019 Feb 11.

Abstract

Esophageal carcinoma, with a increasing incidence, is one of the most aggressive carcinomas in gastrointestinal tract. Epidemiologic studies demonstrate an association of oral pathogens with multiple diseases, including rheumatoid arthritis, cardiovascular diseases, diabetes, and gastrointestinal malignancies. Nevertheless, a causal relationship between oral pathogens and esophageal squamous cell carcinoma (ESCC) has not been elucidated. Here, we found that Porphyromonas was significantly enriched in the saliva of patients with ESCC, compared with that in normal human. In vitro studies showed that Porphyromonas gingivalis (P. gingivalis) promoted the proliferation and motility of ESCC cells, as evidenced by up regulated expression of key molecules implicated in NF-κB signaling pathway. These findings, for the first time, demonstrated a role of oral pathogens in inducing ESCC tumorigenesis and metastasis, which might involve regulation of NF-κB signaling pathway.

Keywords: Esophageal squamous cell carcinoma; Metastasis; NF-κB; Porphyromonas gingivalis; Proliferation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Carcinogenesis / pathology
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • Esophageal Neoplasms / metabolism
  • Esophageal Neoplasms / microbiology
  • Esophageal Neoplasms / pathology*
  • Esophageal Squamous Cell Carcinoma / metabolism
  • Esophageal Squamous Cell Carcinoma / microbiology
  • Esophageal Squamous Cell Carcinoma / pathology*
  • Female
  • Gene Expression Regulation, Neoplastic / physiology
  • Host-Pathogen Interactions / immunology*
  • Humans
  • Male
  • Middle Aged
  • NF-kappa B / genetics
  • Porphyromonas gingivalis / metabolism
  • Porphyromonas gingivalis / physiology*
  • Saliva / microbiology
  • Signal Transduction / genetics*
  • Transcription Factor RelA / genetics
  • Transcription Factor RelA / metabolism*

Substances

  • NF-kappa B
  • RELA protein, human
  • Transcription Factor RelA