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Angiogenesis, Metastasis, and the Cellular Microenvironment

ß1,4-N-Acetylgalactosaminyltransferase III Enhances Malignant Phenotypes of Colon Cancer Cells

Departments of ¹ Surgery and ² Pathology, National Taiwan University Hospital; ³ Department of Plant Pathology and Microbiology, National Taiwan University; and ⁴ Institute of Anatomy and Cell Biology and ⁵ Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan; and ⁶ Animal Technology Institute Taiwan, Miaoli, Taiwan

Requests for reprints: Min-Chuan Huang, Institute of Anatomy and Cell Biology, National Taiwan University College of Medicine, No. 1, Sec. 1 Jen-Ai Road, Taipei 100, Taiwan. Phone: 886-2-2312-3456, ext. 8177; Fax: 886-2-2391-5292. E-mail: mchuang{at}ntu.edu.tw

The enzyme ß1,4-N-acetylgalactosaminyltransferase III (ß4GalNAc-T3) exhibits in vitro activity of synthesizing N,N'-diacetyllactosediamine, GalNAcß1,4GlcNAc. Here, we investigate the expression of ß4GalNAc-T3 in primary colon tumors and the effects of its overexpression on HCT116 colon cancer cells. Real-time reverse transcription-PCR showed that the expression of ß4GalNAc-T3 was up-regulated in 72.5% (n = 40) of primary colon tumors compared with their normal counterparts. ß4GalNAc-T3 overexpression resulted in enhanced cell-extracellular matrix adhesion, migration, anchorage-independent cell growth, and invasion of colon cancer cells. Moreover, ß4GalNAc-T3 overexpression increased tumor growth and metastasis and decreased survival of tumor-bearing nude mice. ß4GalNAc-T3 overexpression showed increased tyrosine phosphorylation of focal adhesion kinase and paxillin Y118 as well as increased extracellular signal–regulated kinase phosphorylation. These results suggest that up-regulation of ß4GalNAc-T3 may play a critical role in promoting tumor malignancy and that integrin and mitogen-activated protein kinase signaling pathways could be involved in the underlying mechanism. (Mol Cancer Res 2007;5(6):543–52)

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