Antitumor activity and underlying mechanism of Sargassum fusiforme polysaccharides in CNE-bearing mice

Int J Biol Macromol. 2018 Jun:112:516-522. doi: 10.1016/j.ijbiomac.2018.01.168. Epub 2018 Jan 31.

Abstract

This study was designed to investigate the antitumor effects of Sargassum fusiforme polysaccharides (SFPS) on nasopharyngeal carcinoma (NPC) and the underlying mechanism of its effect on splenic lymphocytes. As a result, SFPS significantly inhibited the growth of nasopharyngeal carcinoma CNE in vivo, and remarkably increased the serum cytokines and IgM levels in CNE-bearing mice. Meanwhile, SFPS stimulated the peritoneal macrophages to secrete the cytokines, exerted a stimulatory effect on splenic lymphocytes proliferation, and increased the expression of IgM from splenic lymphocytes. The pretreatment of splenic lymphocytes with special antibodies (anti-TLR4 and anti-TLR2) significantly suppressed the proliferation of splenic lymphocytes and blocked SFPS-induced IgM production. SB203580, a specific inhibitor of p38 MAPK, effectively suppressed SFPS-induced IgM secretion in splenic lymphocytes. Taken together, SFPS has antitumor and immunomodulatory activities in NPC, and its activity is mediated, at least in part, by TLR2/TLR4 receptors and p38 MAPK signaling pathway.

Keywords: Antitumor; Immunomodulatory; Nasopharyngeal carcinoma; Sargassum fusiform polysaccharide; Splenic lymphocytes.

MeSH terms

  • Animals
  • Carcinoma / drug therapy*
  • Carcinoma / genetics
  • Carcinoma / pathology
  • Cell Line, Tumor
  • Cell Proliferation / drug effects*
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Mice
  • Nasopharyngeal Carcinoma
  • Nasopharyngeal Neoplasms / drug therapy*
  • Nasopharyngeal Neoplasms / genetics
  • Nasopharyngeal Neoplasms / pathology
  • Polysaccharides / administration & dosage*
  • Polysaccharides / chemistry
  • Polysaccharides / isolation & purification
  • Sargassum / chemistry*
  • Signal Transduction / drug effects
  • Toll-Like Receptor 2 / genetics
  • Toll-Like Receptor 4 / genetics
  • Xenograft Model Antitumor Assays
  • p38 Mitogen-Activated Protein Kinases / genetics

Substances

  • Polysaccharides
  • TLR2 protein, human
  • TLR4 protein, human
  • Toll-Like Receptor 2
  • Toll-Like Receptor 4
  • p38 Mitogen-Activated Protein Kinases