Preliminary studies of β3GnT families expression regulated by a SRC inhibitor

• Main Authors: Hsuan-Chen Liu, 劉軒辰
• Other Authors: Kuo Yuan Hwa
• Format: Others
• Language: en_US
• Published: 2012
• Online Access: http://ndltd.ncl.edu.tw/handle/7q86v8

碩士 === 國立臺北科技大學 === 有機高分子研究所 === 100 === The β1,3-N-acetylglucosaminyltransferase(β3GnT) protein family is responsible for the synthesis of β1,3-Linked GlcNAc residues to different specific types of glycoconjugates of cells. The β3GnT protein family is one of the important enzyme family in glycosylation, and the β3GnT genes were widely expressed in human and mouse tissues. Some members of the protein family are involved in the biosynthesis of poly-N-acetyllactosamine chains, which has been implicated for their metastatic potential in tumor cells. In addition, SRC is a well-known oncogene, which has been implicated in pathways regulating cell proliferation, angiogenesis, invasion and metastasis. Therefore, the goal of my thesis is to study if mouse/and human β3GnT genes is under the control of SRC. First, we had used a stable mouse cell line expressing v-Src, we found SRC overexpressed mouse cell line displayed the increase of poly-N-acetyllactosamine in comparing with the normal NIH/3T3 cell line. To further study the regulatory role of SRC on the poly-N-acetyllactosamine and β3GnT genes, we had studied the expressions of β3GnTs in human colon cancer SW620 cells and lung cancer NCI-H23 cells by treating the cells with bosutinib, a SRC inhibitor. The real-time qPCR results showed that when cancer cell line was treated with bosutinib affected the expression of the transcripts of the β3GnT2, β3GnT3, β3GnT4, β3GnT5, β3GnT6 and β3GnT8 in NCI-H23, and the β3GnT3, β3GnT6 and β3GnT8 in SW620. Furthermore, the FACS analysis revealed that the surface expression of poly-N-acetyllactosamine was altered by the SRC inhibitor, which was consistent with the results from the gene expression of β3GnT2 and β3GnT8. As a summary, we had demonstrated at least β3GnT2 and β3GnT8 were under the control of SRC pathway, which resulted in alteration of expression of poly-N-acetyllactosamine.