Journal
FEBS LETTERS
Volume 582, Issue 23-24, Pages 3415-3422Publisher
WILEY
DOI: 10.1016/j.febslet.2008.09.004
Keywords
Hepatocyte growth factor; Met oncogene; Nasopharyngeal cancer; Signaling; Invasion; Cell motility
Funding
- Committee on Research and Conference Council [HKU 200607176117, 200707176141]
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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.
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