Journal
CELL CYCLE
Volume 15, Issue 7, Pages 886-894Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2016.1152428
Keywords
EMT; HGF/c-Met; hepatocellular carcinoma; HSCs; invasion and migration; p53
Categories
Funding
- Key Basic Research Project of China [2012CBA01303]
- National Natural Science Foundation of China [81372312, 81472737, 81402018, 81402020, 81401308, 81402026, 81372330, 81572444, 81502417, 81502543, 81221061]
- Special Funds for National Key Sci-Tech Sepcial Project of China [2016ZX10002019-005-002]
- Shanghai Science and Technology Committee [14ZD1900403, 14ZR1409200, 15PJ1410600]
- Shanghai Municipal Education Commission [14ZZ086]
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The biological behaviors of hepatocellular carcinoma (HCC) are complex mainly due to heterogeneity of progressive genetic and epigenetic mutations as well as tumor environment. Hepatocyte growth factor (HGF)/c-Met signaling pathway is regarded to be a prototypical example for stromal-epithelial interactions during developmental morphogenesis, wound healing, organ regeneration and cancer progression. And p53 plays as an important regulator of Met-dependent cell motility and invasion. Present study showed that 2 HCC cell lines, Hep3B and HepG2, displayed different invasive capacity when treated with HGF which was secreted by hepatic stellate cells (HSCs). We found that HGF promoted Hep3B cells invasion and migration as well as epithelial-mesenchymal transition (EMT) occurrence because Hep3B was p53 deficient, which leaded to the c-Met over-expression. Then we found that HGF/c-Met promoted Hep3B cells invasion and migration by upregulating Snail expression. In conclusion, HGF/c-Met signaling is enhanced by loss of p53 expression, resulting in increased ability of invasion and migration by upregulating the expression of Snail.
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