URN |
etd-0824111-001511 |
Author |
Ping-Hsuan Wu |
Author's Email Address |
bingshiuan21@gmail.com |
Statistics |
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Department |
Biological Sciences |
Year |
2010 |
Semester |
2 |
Degree |
Master |
Type of Document |
|
Language |
English |
Title |
The role of LECT2 in liver carcinogenesis |
Date of Defense |
2011-07-01 |
Page Count |
62 |
Keyword |
Wnt pathway
β-catenin
Hepatocellular carcinoma
cellular signaling
LECT2
|
Abstract |
Leukocyte cell-derived chemotaxin 2 (LECT2) is first isolated as a 16-kDa secreted protein from cultured fluid of phytohemagglutinin-activated human T-cell leukemia SKW-3 cells. Recently LECT2 has shown to be synthesized by human hepatocytes and stimulates the growth of chondrocytes. LECT2 is involved in chemotactic factor to neutrophils and may be associated with rheumatoid arthritis. Besides, LECT2 is evolutionarily conserved and acts as a repressor in the Wnt/β-catenin signaling pathway. Wnt/β-catenin signaling is implicated in liver carcinogenesis. However, the exact roles of LECT2 in liver carcinogenesis are not yet well characterized. This study is to investigate the extra roles of LECT2 in Wnt signaling. Our results showed that adenoviral administration of LECT2 over-expression suppress oncogenic processes such as migration, invasion, proliferation and colony formation, as well as alteration in cell cycle distributions. In animal model significantly suppress liver malignancies in orthotopic Novikoff hepatoma. In conclusion, we show that ad-LECT2 gene delivery attenuated cell carcinogenesis process via downregulated Wnt/β-catenin signaling in vitro and suppressed tumor growth in vivo. Besides LECT2 over-expression represents a novel therapeutically factor for hepatocelluar carcinoma. |
Advisory Committee |
Cheng, Jiin-Tsuey - chair
Hu, Tsung-Hui - co-chair
Tai, Ming-Hong - advisor
|
Files |
indicate access worldwide |
Date of Submission |
2011-08-24 |