Biglycan enhances gastric cancer invasion by activating FAK signaling pathway

Oncotarget. 2014 Apr 15;5(7):1885-96. doi: 10.18632/oncotarget.1871.

Abstract

Biglycan (BGN) is an important member of small leucine-rich proteoglycans family, and has been implicated in oncogenesis and development of various human cancer types. Here we report that BGN promotes tumor invasion and metastasis of gastric cancer both in vitro and in vivo. BGN expression is significantly higher in gastric cancer tissues and associated with lymph node metastasis, depth of tumor invasion and TNM stage. BGN enhances gastric cancer cell wound healing, migration and invasion ability as well as the tube formation ability of endothelial cells in vitro. Animal experiments results in vivo are consistent with outcomes in vitro. BGN induces increased phosphorylation of FAK (Tyr576/577, Tyr925 and Tyr397) and Paxillin. These results indicate that BGN is upregulated, and plays an oncogenic role, in gastric cancer metastasis by activating the FAK signaling pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Animals
  • Biglycan / physiology*
  • Cell Line, Tumor
  • Cell Movement
  • Endothelial Cells / physiology
  • Female
  • Humans
  • Male
  • Mice
  • Mice, Nude
  • Middle Aged
  • Neoplasm Invasiveness
  • Neoplasm Staging
  • Paxillin / metabolism
  • Peptides / metabolism*
  • Phosphorylation
  • RNA, Messenger / analysis
  • Signal Transduction
  • Stomach Neoplasms / genetics
  • Stomach Neoplasms / metabolism
  • Stomach Neoplasms / pathology*
  • Up-Regulation*
  • Wound Healing

Substances

  • Biglycan
  • FAK peptide
  • Paxillin
  • Peptides
  • RNA, Messenger