tailieunhanh - Báo cáo khoa học: Insulin/protein kinase B signalling pathway upregulates metastasis-related phenotypes and molecules in H7721 human hepatocarcinoma cell line

The effect of insulin on cancer metastatic potential was studied in a human hepatocarcinoma cell line, H7721. Cell adhesion to human umbilical vein endothelial cells (HUVECs) and lamininaswell as chemotactic cellmigration and invasion were selected as the indices of metastasis-related phenotypes for assessment of metastatic potential ex vivo. The results indicated that insulin enhanced all of these metastasis-related phenotypes. After the cells were treated with specific inhibitor of PI3K (LY294002) or transfected with antisense cDNA of PKB (AS-PKB), all of the above phenotypes were attenuated, and they could not be significantly stimulated by insulin, indicating that the insulin effect onmetastatic potential was mediated by PI3K and PKB. . | Eur. J. Biochem. 270 3795-3805 2003 FEBS 2003 doi Insulin protein kinase B signalling pathway upregulates metastasis-related phenotypes and molecules in H7721 human hepatocarcinoma cell line Hui-Ling Qi Ying Zhang Jun Ma Peng Guo Xia-Ying Zhang and Hui-Li Chen Key Laboratory of Glycoconjugate Research Ministry of Health Department of Biochemistry Shanghai Medical College of Fu-Dan University Shanghai China The effect of insulin on cancer metastatic potential was studied in a human hepatocarcinoma cell line H7721. Cell adhesion to human umbilical vein endothelial cells HUVECs and laminin as well as chemotactic cell migration and invasion were selected as the indices of metastasis-related phenotypes for assessment of metastatic potential ex vivo. The results indicated that insulin enhanced all of these metastasis-related phenotypes. After the cells were treated with specific inhibitor of PI3K LY294002 or transfected with antisense cDNA of PKB AS-PKB all of the above phenotypes were attenuated and they could not be significantly stimulated by insulin indicating that the insulin effect on metastatic potential was mediated by PI3K and PKB. Only the monoclonal antibody to the sialyl Lewis X SLex but not antibodies to other Lewis antigens significantly blocked the cell adhesion to HUVECs cell migra tion and invasion suggesting that SLex played a crucial role in the metastatic potential of H7721 cells. The upregulation of cell surface SLex and 7-1 3-fucosyltransferase-VII a-1 3 Fuc T-VII enzyme for SLex synthesis was also mediated by PI3K and PKB since LY294002 and AS-PKB also reduced the expressions of SLex and a-1 3 FucT-VII and attenuated the response to insulin. Furthermore the alterations in the expressions of PKB protein and activity were correlated to the changes of metastatic phenotypes and SLex expression. Taken together the insulin PKB signalling pathway participated in the enhancement of metastatic potential of H7721 cells which

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