Hepatocyte growth factor enhances proteolysis and invasiveness of human nasopharyngeal cancer cells through activation of PI3K and JNK

Hong Yan Zhou, Kai Fung Wan, Carman K.M. Ip, Chris K C WONG, Nai Ki MAK, Kwok Wai Lo, Alice S.T. Wong*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

31 Citations (Scopus)

Abstract

The hepatocyte growth factor (HGF) receptor, Met, is frequently overexpressed in nasopharyngeal cancer (NPC). Here, we showed for the first time that human NPC cells with high Met expression were more sensitive to the cell motility and invasion effect of HGF. The downregulation of Met by small interfering RNA decreased tumor cell invasion/migration. HGF significantly increased matrix metalloproteinase-9 production. This was inhibited by blocking phosphatidylinositide 3-kinase (PI3K) and c-Jun N-terminal kinase (JNK), but not extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase signaling pathways. We also demonstrated that PI3K induced activation of JNK, with Akt as a potential point of this cross-talk. These results provide new insights into the molecular mechanism responsible for NPC progression and metastasis.

Original languageEnglish
Pages (from-to)3415-3422
Number of pages8
JournalFEBS Letters
Volume582
Issue number23-24
DOIs
Publication statusPublished - 15 Oct 2008

Scopus Subject Areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

User-Defined Keywords

  • Cell motility
  • Hepatocyte growth factor
  • Invasion
  • Met oncogene
  • Nasopharyngeal cancer
  • Signaling

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