https://scholars.lib.ntu.edu.tw/handle/123456789/596193
標題: | β1,4-N-acetylgalactosaminyltransferase III enhances malignant phenotypes of colon cancer cells | 作者: | JOHN HUANG JIN-TUNG LIANG Hsiu-Chin Huang Shen, Tang-Long Hsiao-Yu Chen NENG-YU LIN Mei-Ieng Che WEI-CHOU LIN MIN-CHUAN HUANG |
公開日期: | 2007 | 卷: | 5 | 期: | 6 | 起(迄)頁: | 543-552 | 來源出版物: | Molecular Cancer Research | 摘要: | The enzyme β1,4-N-acetylgalactosaminyltransferase III (β4GalNAc-T3) exhibits in vitro activity of synthesizing N,N′-diacetyllactosediamine, GalNAcβ1,4GlcNAc. Here, we investigate the expression of β4GalNAc-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 β4GalNAc-T3 was up-regulated in 72.5% (n = 40) of primary colon tumors compared with their normal counterparts. β4GalNAc-T3 overexpression resulted in enhanced cell-extracellular matrix adhesion, migration, anchorage-independent cell growth, and invasion of colon cancer cells. Moreover, β4GalNAc-T3 overexpression increased tumor growth and metastasis and decreased survival of tumor-bearing nude mice. β4GalNAc-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 β4GalNAc-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. Copyright ? 2007 American Association for Cancer Research. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-34250892600&doi=10.1158%2f1541-7786.MCR-06-0431&partnerID=40&md5=ae92f93dc08f2a08a1c913ad813e3d93 https://scholars.lib.ntu.edu.tw/handle/123456789/596193 |
ISSN: | 1541-7786 | DOI: | 10.1158/1541-7786.MCR-06-0431 | SDG/關鍵字: | beta1,4 n acetylgalactosaminyltransferase III; focal adhesion kinase; mitogen activated protein kinase; paxillin; transferase; unclassified drug; antineoplastic agent; beta 1,4 N acetylgalactosaminyltransferase III, human; beta-1,4-N-acetylgalactosaminyltransferase III, human; n acetylgalactosaminyltransferase; paxillin; anchorage independent growth; animal experiment; animal model; animal tissue; article; cancer cell culture; cancer invasion; cancer survival; cell adhesion; cell invasion; cell migration; colon cancer; controlled study; enzyme phosphorylation; extracellular matrix; female; gene overexpression; human; human cell; malignant neoplastic disease; metastasis; mouse; nonhuman; phenotype; priority journal; protein function; real time polymerase chain reaction; reverse transcription polymerase chain reaction; tumor promotion; upregulation; animal; cell proliferation; colon tumor; gene expression regulation; metabolism; nude mouse; pathology; phenotype; physiology; tumor cell line; Mus musculus; Animals; Antineoplastic Agents; Cell Line, Tumor; Cell Proliferation; Colonic Neoplasms; Focal Adhesion Protein-Tyrosine Kinases; Gene Expression Regulation, Neoplastic; Humans; Mice; Mice, Nude; N-Acetylgalactosaminyltransferases; Neoplasm Invasiveness; Neoplasm Metastasis; Paxillin; Phenotype |
顯示於: | 病理學科所 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。