Title page for etd-0211111-023201


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URN etd-0211111-023201
Author Li-na Yi
Author's Email Address No Public.
Statistics This thesis had been viewed 5567 times. Download 973 times.
Department Biological Sciences
Year 2010
Semester 1
Degree Master
Type of Document
Language English
Title Overexpression of Manganese Superoxide Dismutase (SOD2) Inhibited the Tumorigenicity of Hepatoma Cells
Date of Defense 2010-07-16
Page Count 61
Keyword
  • Hydrogen peroxide
  • reactive oxygen species
  • Mn superoxide dismutase
  • Hepatocellular carcinoma
  • superoxide anions
  • Abstract Hepatocellular carcinoma (HCC) is one of the most common and devastating malignant tumors in Taiwan. Due to an imbalanced between reactive oxygen species (ROS) production and detoxification, oxidative stress, has been implicated in liver carcinogenesis. Superoxide dismutases (SODS) play a key role in the detoxification of superoxide radicals and thus protect cells from damage induced by free radicals. Manganese superoxide dismutase (MnSOD or SOD2) is a member of the superoxide dismutase family located in mitochondria. SOD2 transforms toxic superoxide, a byproduct of the mitochondrial electron transport chain, into hydrogen peroxide and diatomic oxygen. Though reduced SOD2 protein level and activities have been reported in hepatoma tissues, it remains unclear how SOD2 expression affected the tumorigenic processes of hepatoma cells. Expression analysis of an array of human HCC cell lines revealed that SOD2 were down-regulated in poorly differentiated SK-Hep-1 hepatoma cells. Moreover, SOD2 is downregulated in 68.8% of resected HCC samples (97 out of 141 cases). Adenovirus-mediated SOD2 gene delivery increased the cellular SOD2 protein level and H2O2 production, but reduced the superoxide anion level in SK-Hep-1 cells. Furthermore, SOD2 restoration significantly reduced the proliferation, motility, and colony formation of SK-Hep-1 cells. In vivo animal model, the finding of SOD2 overexpression inhibited the proliferation of Sk-Hep-1 hepatoma cells while reduced the tumor growth in mice. Flow cytometry analysis showed that SOD2 gene transfer inhibited the growth of hepatoma cells through induction of cell cycle arrest at G2/M phase. This was associated with declined cdc2/cdk1 and cyclin B1 expression and upregulation p21Cip1 by SOD2 gene delivery. However, SOD2 overexpression had no effect on the secretion of matrix metalloproteinase-2 (MMP-2) and MMP-9.In conclusion, SOD2 overexpression suppresses the tumorigenicity of hepatoma cells and may hold promise for HCC treatment.
    Advisory Committee
  • Ching-Mei Hsu - chair
  • Tsung-Hui Hu - co-chair
  • Ming-Hong Tai - advisor
  • Files
  • etd-0211111-023201.pdf
  • indicate in-campus access immediately and off_campus access in a year
    Date of Submission 2011-02-11

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