Plantamajoside inhibits lipopolysaccharide-induced epithelial-mesenchymal transition through suppressing the NF-κB/IL-6 signaling in esophageal squamous cell carcinoma cells

Biomed Pharmacother. 2018 Jun:102:1045-1051. doi: 10.1016/j.biopha.2018.03.171. Epub 2018 Apr 5.

Abstract

Plantamajoside (PMS) is a major compound of Plantago asiatica and possesses anti-tumor activity. However, the effect of PMS on esophageal squamous cell carcinoma (ESCC) and the underlying mechanism of action are unclear. The present study aimed to evaluate the effect of PMS on lipopolysaccharide (LPS)-induced epithelial-mesenchymal transition (EMT) in ESCC. The results showed that PMS inhibited viability of ESCC cell lines (Eca-109 and TE-1) in a concentration-dependent manner. PMS also inhibited LPS-induced EMT in ESCC cells. PMS inhibited LPS-induced activation of the NF-κB pathway and IL-6 expression. PMS also suppressed IL-6-induced EMT in ESCC cells. Treatment of BAY11-7082 (an inhibitor of NF-κB) or antibody against IL-6 alleviated the effect of LPS-induced EMT in ESCC cells. Besides, inhibition of NF-κB decreased IL-6 expression. In conclusion, the results indicated that PMS inhibited LPS-induced EMT through suppressing the NF-κB/IL-6 signaling in ESCC cell lines, suggesting that PMS might be a useful agent for the treatment of ESCC.

Keywords: Epithelial-mesenchymal transition; Esophageal squamous cell carcinoma; IL-6; NF-κB; Plantamajoside.

MeSH terms

  • Carcinoma, Squamous Cell / drug therapy*
  • Carcinoma, Squamous Cell / genetics
  • Carcinoma, Squamous Cell / pathology*
  • Catechols / chemistry
  • Catechols / pharmacology
  • Catechols / therapeutic use*
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Epithelial-Mesenchymal Transition* / drug effects
  • Epithelial-Mesenchymal Transition* / genetics
  • Esophageal Neoplasms / drug therapy*
  • Esophageal Neoplasms / genetics
  • Esophageal Neoplasms / pathology*
  • Esophageal Squamous Cell Carcinoma
  • Gene Expression Regulation, Neoplastic / drug effects
  • Glucosides / chemistry
  • Glucosides / pharmacology
  • Glucosides / therapeutic use*
  • Humans
  • Interleukin-6 / metabolism*
  • Lipopolysaccharides
  • NF-kappa B / metabolism*
  • Signal Transduction* / drug effects
  • Signal Transduction* / genetics

Substances

  • Catechols
  • Glucosides
  • Interleukin-6
  • Lipopolysaccharides
  • NF-kappa B
  • plantamajoside