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Extension of poly‐N‐acetyllactosamine chain in human cancer cell lines is under src regulation
Author(s) -
Hwa KuoYuan,
Liu Hsuan-Chen,
Chou Teh-Ying
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.607.2
Subject(s) - proto oncogene tyrosine protein kinase src , cell culture , metastasis , bosutinib , oncogene , cancer research , cancer cell , cell , biology , microbiology and biotechnology , cancer , chemistry , phosphorylation , cell cycle , signal transduction , genetics , tyrosine kinase , nilotinib
Alternation of glycan synthesis is an important process in cancer metastasis. And, the extent of poly‐N‐acetyllactosamine chains on tumor cells has been implicated for their metastatic potential. β1,3‐N‐acetylglucosamonyltransferase‐2 (β3GnT2) and β1,3‐N‐acetylglucosamonyltransferase‐8 (β3GnT8) are two of the glycosyltransferases responsible for the synthesis of poly‐N‐acetyllactosamine. Since Src is a well‐known oncogene, which has been implicated in pathways regulating cell proliferation, angiogenesis, invasion and metastasis, we had generated a stable mouse cell line expressing v‐Src. First, we had examined the expression of the two genes in stable transformed v‐Src and wild‐type NIH/3T3 cell lines. And, we found that the cell line with overexpressed Src had higher level β3GnT8 transcripts than the normal NIH/3T3 cell line. To further illustrate the regulatory role of Src on the two genes, we had investigated the expressions of β3GnT2 and β3GnT8 in SW620 and H23 by treating the cells with bosutinib, a Src inhibitor. We found that the decrease of the expression of β3GnT2 was not significant, but the expression of β3GnT8 was significantly decreased by the Src inhibitor. Furthermore, we had found that the surface expression of poly‐N‐acetyllactosamine was altered by the Src inhibitor, by FACS analysis. This work is supported by the National Taipei University of Technology to KYH (NTUT 100‐140‐01, NTUT 99‐140‐04).