?-1,3-Fucosyltransferase-VII stimulates the growth of hepatocarcinoma cells via the cyclin-dependent kinase inhibitor p27Kip1

Wang, Q. Y.; Guo, Peng; Duan, Lingling; Shen, Zhemin; Chen, H. L.

doi:10.1007/s00018-004-4349-8

Cited by 19 publications

(22 citation statements)

References 23 publications

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“…We further explored the biological changes of LOVO cells after stable transfection of FucT-VII in vitro. Previous studies showed that the tranfection of FucT-VII into H7721 hepatocarcinoma cells could enhance phosphorylation of retinoblastoma (Rb) protein and facilitate the G1/S transition and growth rate of the cells through the regulation of CDI Kipl protein (31). In our study, we transfected ·1,3 FucT-VII into human colon cancer cells and yielded a similar result.…”

Section: Discussionsupporting

confidence: 71%

α1,3 Fucosyltransferase VII plays a role in colorectal carcinoma metastases by promoting the carbohydration of glycoprotein CD24

Zhang

Luo

et al. 2010

Oncol Rep

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Abstract. Changes in the expression levels of ·1,3 FucT-VII and carbohydrate product SLe X have been reported in certain types of malignant transformations. However, the specific role of FucT-VII in human colorectal carcinoma is still not clear. We evaluated the expression of FucT-VII in tumor specimens from 30 colorectal carcinoma patients by RT-PCR and immunohistochemistry. The alteration of metastatic potential of LOVO cells before and after ·1,3 FucT-VII gene transfection was also assayed. The expression change of glycoprotein CD24 and carbohydrate antigen SLe X after stable transfection of LOVO was also examined in vitro. Higher mRNA and protein expression of FucT-VII were observed in colorectal tumors compared with adjacent normal ones. The cell chemotactic migration and invasion were enhanced after ·1,3 FucT-VII transfection in LOVO cells. There was a positive correlation between ·1,3 FucT-VII mRNA expression and lymph node status (p=0.009) and AJCC stage (p=0.007), similar correlation was also observed at protein level (p=0.042 and 0.022, respectively). Overexpression of ·1,3 FucT-VII promoted the expression of CD24 and SLe X in LOVO cells. Our findings suggest that ·1,3 FucT-VII might play a role in colorectal carcinoma metastases by promoting the carbohydration of glycoprotein CD24.

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Section: Discussionsupporting

confidence: 71%

α1,3 Fucosyltransferase VII plays a role in colorectal carcinoma metastases by promoting the carbohydration of glycoprotein CD24

Zhang

Luo

et al. 2010

Oncol Rep

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“…In addition to the MAPKs, another protein kinase Akt is able to mediate cell growth via the phosphorylation of a variety of substrates (Cicenas, 2008;de Souza et al, 2009). Many studies have implicated the regulating MAPK and PI3K/Akt signaling as likely mechanisms for regulation of cell cycle in human cancer cells by glycosyltransferases (Wang et al, 2005;Wang et al, 2007). However, limited information is available on the significance of MAPK and PI3K/Akt pathway as potential targets for FUT4.…”

Section: Discussionmentioning

confidence: 98%

Overexpression of fucosyltransferase IV promotes A431 cell proliferation through activating MAPK and PI3K/Akt signaling pathways

Yang¹,

Liu²,

Liu³

et al. 2010

Journal Cellular Physiology

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Lewis Y (LeY) is a carbohydrate tumor-asssociated antigen. The majority of cancer cells derived from epithelial tissue express LeY type difucosylated oligosaccharide. Fucosyltransferase IV (FUT4) is an essential enzyme that catalyzes the synthesis of LeY oligosaccharide. Our previous studies have shown that FUT4 overexpression promotes A431 cell proliferation, but the mechanism is still largely unknown. Herein, we investigated the role of the mitogen-activated protein kinases (MAPKs) and phosphoinositide-3 kinase (PI3K)/Akt signaling pathways on FUT4-induced cell proliferation. Results show that overexpression of FUT4 increases the phosphorylation of ERK1/2, p38 MAPK, and PI3K/Akt. Inhibitors of PI3K (LY294002 and Wortmannin) prevented the phosphorylation of ERK1/2, p38 MAPK, and Akt PI3K). Moreover, phosphorylation of Akt is abolished by inhibitors of ERK1/2 (PD98059) and p38 MAPK (SB203580). These data suggested that FUT4 not only activates MAPK and PI3K/Akt signals, but also promotes the crosstalk among these signaling pathways. In addition, FUT4-induced stimulation of cell proliferation correlates with increased cell cycle progression by promoting cells into S-phase. The mechanism involves in increased expression of cyclin D1, cyclin E, CDK 2, CDK 4, and pRb, and decreased level of cyclin-dependent kinases inhibitors p21 and p27, which are blocked by the inhibitors of upstream signal molecules, MAPK and PI3K/Akt. In conclusion, these studies suggest that FUT4 regulates A431 cell growth through controlling cell cycle progression via MAPK and PI3K/Akt signaling pathways.

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“…28,29 Accordingly and having shown that FUT1 selectively and quantitatively inhibits sLe x synthesis in HepG2 cells, we investigated the capacity of FUT1-expressing cells to develop tumors. To this end, cells were subcutaneously inoculated to nu/nu nude mice and results from two independent experiments, using 12 animals per each experiment, are shown in Figure 2.…”

Section: Fut1 Strongly Inhibits Tumor Formation In Nude Micementioning

confidence: 99%

Introducing α(1,2)‐linked fucose into hepatocarcinoma cells inhibits vasculogenesis and tumor growth

Mathieu¹,

Gerolami²,

Luis³

et al. 2007

Intl Journal of Cancer

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The glycoantigen sialyl-Lewis x (sLex) and its isomer sialy-Lewis a (sLea) are frequently associated with advanced states of cancer and metastasis. In a previous work, we have shown that hepatocarcinoma cells (HCC) HepG2 interact with the endothelial Eselectin exclusively through sLe x oligosaccharides, the synthesis of which could be completely prevented by the a(1,2)-fucosyltransferase-I (FUT1), thus resulting in a strong inhibition of adhesion and rolling on activated endothelial cells. The purpose of the present study was to evaluate the impact of inhibiting sLex synthesis and the subsequent E-selectin adhesion, on HCC tumor growth in nude mice. Four weeks after subcutaneous transplantation of cells, no FUT1-derived tumor could be detected, whereas 75% of control animals developed large size tumor nodules. Between the 4th and the 8th week postinoculation, 33% tumors arose from FUT1-transduced cells but showed a slow growth (nodule volumes less than 500 mm 3 ), while more than 50% of control tumors reached volumes between 1,500 and 3,000 mm 3 . Several parameters were examined, including cell division and proliferation, apoptosis, adhesion to extracellular matrix components and angiogenesis/vasculogenesis. We provide evidence that among all, vasculogenesis was the most clearly affected by FUT1 expression, suggesting that tumor angiomorphogenesis may, at least partly, depend on Eselectin-mediated interaction between HCC and endothelial cells, the inhibition of which remarkably retards tumor growth. ' 2007 Wiley-Liss, Inc.Key words: a(1,2)-fucosyltransferase-I; E-selectin; sialyl-Lewis; antitumor; vasculogenesisThe sialyl-Lewis antigens (sLex and sLea) are blood grouprelated antigens naturally expressed on leukocytes to initiate leukocyte-endothelium interaction mediated by the cytokine-inducible endothelial adhesion molecule E-selectin. 1,2 In addition to this physiological role in inflammation, sialyl-Lewis antigens are also considered as tumor markers expressed on many cancer cells and therefore, they are thought to be involved in metastasis by initiating tumor cell-endothelium adhesion. 3 Indeed, the expression of sialyl-Lewis antigens on carcinoma cells is frequently associated with advanced states of cancer and a statistically relevant relationship has been established between the postoperative prognosis of patients and the degree of expression of sialyl-Lewis antigens on cancer tissues. 3 Besides, several lines of evidence from selectin-deficient mice studies pointed out the contribution of selectins in facilitating tumor growth and progression. 4,5 In particular, E-selectin and its sLex-containing glycoconjugate ligands have been shown to be involved in the essential events of tumor angiogenesis, 6-9 including the fact that coinjection of tumor cells expressing high level of sLe x together with endothelial cells constitutively expressing E-selectin, has been found to promote tumor angiogenesis and growth. 10 We have recently succeeded in strongly blocking the expression of sLex on digestive cancer cells...

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?-1,3-Fucosyltransferase-VII stimulates the growth of hepatocarcinoma cells via the cyclin-dependent kinase inhibitor p27Kip1

Cited by 19 publications

References 23 publications

α1,3 Fucosyltransferase VII plays a role in colorectal carcinoma metastases by promoting the carbohydration of glycoprotein CD24

α1,3 Fucosyltransferase VII plays a role in colorectal carcinoma metastases by promoting the carbohydration of glycoprotein CD24

Overexpression of fucosyltransferase IV promotes A431 cell proliferation through activating MAPK and PI3K/Akt signaling pathways

Introducing α(1,2)‐linked fucose into hepatocarcinoma cells inhibits vasculogenesis and tumor growth

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