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URN	etd-0824111-001511
Author	Ping-Hsuan Wu
Author's Email Address	bingshiuan21@gmail.com
Statistics	This thesis had been viewed 5576 times. Download 687 times.
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	etd-0824111-001511.pdf indicate access worldwide
Date of Submission	2011-08-24

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