Hepatocellular carcinoma (HCC) is one of the most prevalent cancers in
Taiwan. Copper-zinc superoxide dismutase (SOD1) is widely distributed and
comprises 90% of the total superoxide dismutase (SOD), which catalyzes the
conversion of superoxide to hydrogen peroxide. Reduced expression of
antioxidant enzymes, particularly SOD1, has been identified in human
hepatoma specimens and cell lines. However, it remains unclear how SOD1
expression affected the tumorigenic processes of hepatoma cells. Expression
analysis of an array of human HCC cell lines revealed that SOD1 protein
levels were down regulated in poorly differentiated SK-Hep-1 cells.
Adenovirus-mediated SOD1 expression increased the SOD1 protein level by
30-40% of control. In addition, SOD1 gene transfer decreased the cellular
O2
¡V level yet increased the H2O2 production. SOD1 overexpression
significantly reduced the proliferation, motility, and anchorage-independent
growth of SK-Hep-1 cells, but had no effect on the secretion of matrix
metalloproteinase-2 (MMP-2) and MMP-9. SOD1 restoration inhibited the
proliferation of SK-Hep-1 cells through induction of cell cycle arrest, which
was associated with decreased expression of cyclin A, cyclin D1, cdk1, cdk4
and upregulation of p21Cip1 and p27kip1. Besides, SOD1 overexpression also
inhibited the nuclear factor £e B (NF-£eB) activities, thereby attenuating the
proliferation and migration of SK-Hep-1 cells. In conclusion, SOD1
restoration attenuated the tumorigenicity of hepatoma cells.
| Identifer | oai:union.ndltd.org:NSYSU/oai:NSYSU:etd-0828107-170446 |
| Date | 28 August 2007 |
| Creators | Lin, I-Chun |
| Contributors | Ming-Hong Tai, Tsung-Hui Hu, Chung-Lung Cho |
| Publisher | NSYSU |
| Source Sets | NSYSU Electronic Thesis and Dissertation Archive |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0828107-170446 |
| Rights | not_available, Copyright information available at source archive |
Page generated in 0.0016 seconds