Suppression by ganglioside GD1A of migration capability, adhesion to vitronectin and metastatic potential of highly metastatic FBJ-LL cells

Hyuga, Sumiko; Yamagata, Sadako; Takatsu, Yoshihiro; Hyuga, Masashi; Nakanishi, Hayao; Furukawa, Koichi; Yamagata, Toshio

doi:10.1002/(sici)1097-0215(19991126)83:5<685::aid-ijc20>3.0.co;2-4

Cited by 31 publications

(14 citation statements)

References 17 publications

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“…For both cell types, the low motility variants are characterized by high ganglioside and high caveolin-1 expression, although the high motility variants contain low ganglioside and low caveolin-1 levels. Treatment of the highly motile FBJ-LL osteosarcoma cell line with exogenous GD1a ganglioside or transfection with GM2/GD2 synthase cDNA resulted in the up-regulation of caveolin-1 expression with reduced metastatic potential and suppressed cell adhesion to vitronectin (57). Similarly, GM3 synthase-transfected A2780 ovarian carcinoma cells were characterized by an increased expression of caveolin-1 and reduced in vitro cell motility.…”

Section: Discussionmentioning

confidence: 98%

A Glycosphingolipid/Caveolin-1 Signaling Complex Inhibits Motility of Human Ovarian Carcinoma Cells

Prinetti

Cao

Illuzzi

et al. 2011

Journal of Biological Chemistry

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Background: Altered cell motility is a crucial aspect determining the invasiveness of tumors. Results: Cells with concomitantly high levels of gangliosides and caveolin-1 have reduced activation of Src and reduced motility. Conclusion: A caveolin-1⅐glycolipid complex can modulate the motility of tumor cells by regulating Src activity Significance: This is a novel mechanism for the control of cell motility by caveolin-1 and gangliosides.

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Section: Discussionmentioning

confidence: 98%

A Glycosphingolipid/Caveolin-1 Signaling Complex Inhibits Motility of Human Ovarian Carcinoma Cells

Prinetti

Cao

Illuzzi

et al. 2011

Journal of Biological Chemistry

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“…8 Thus the effect of GD1a expression on 100 ng/ml HGF-induced migration was investigated by using poorly metastatic FBJ-S1 cells expressing a high level of GD1a, highly metastatic FBJ-LL cells expressing a low level of GD1a and transfectants expressing GD1a at various levels. 7 The HGFinduced motility of FBJ-S1 cells was one-thirtieth that of FBJ-LL cells (Fig. 1a).…”

Section: Effect Of Gd1a Expression On Hgf-induced Migrationmentioning

confidence: 89%

“…13 These cells were cultured in medium containing RPMI-640 (Nissui, Tokyo, Japan) supplemented with 10% FCS (GIBCO BRL, Grand Island, NY) at 37°C in a humidified atmosphere of 95% air and 5% CO 2 . GM2/GD2-synthase cDNA transfectants (LA5-7 and LA5-22) and mock-transfectant M-5 cell 7 were cultured in RPMI-1640 supplemented with 10% FCS and 100 g/ml Geneticin (GIBCO BRL). HepG2 cells, a human hepatoma cell line, were cultured in DMEM (Sigma, St. Louis, MO) with 10% FCS at 37°C in a humidified atmosphere of 95% air and 5% CO 2 .…”

Section: Cell Lines and Culturementioning

confidence: 99%

“…DISCUSSION We previously reported that the metastatic potential of FBJ-LL cells was completely suppressed by enforced GD1a expression. 7 Thus, GD1a is an important molecule in metastasis and its mechanism needs to be clarified. In the present study, we showed that GD1a inhibited HGF-induced motility in different cancer cells and suppressed tyrosine phosphorylation of c-Met.…”

Section: Level Of C-met Tyrosine Phosphorylation In Gd1a-pretreated Hmentioning

confidence: 99%

“…6 GD1a inhibited the serum-induced motility of FBJ-LL cells and the metastatic potential of FBJ-LL cells was completely suppressed by enforced GD1a expression. 7 It is possible that GD1a suppresses metastasis of FBJ-LL cells by inhibiting cell migration. The target molecules of GD1a need to be identified to clarify the mechanism of inhibition of metastasis by GD1a.…”

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Ganglioside GD1a inhibits HGF-induced motility and scattering of cancer cells through suppression of tyrosine phosphorylation of c-Met

Hyuga¹,

Kawasaki²,

Hyuga³

et al. 2001

Int. J. Cancer

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We previously reported that ganglioside GD1a, which is highly expressed in poorly metastatic FBJ-S1 cells, inhibits the serum-induced motility of FBJ-LL cells and that the metastatic potential of FBJ-LL cells is completely suppressed by enforced GD1a expression (Hyuga et al., Int J Cancer 1999; 83:685-91). We recently discovered that hepatocyte growth factor (HGF) induces FBJ-LL cell motility. In the present study, the HGF-induced motility of FBJ-S1 cells was found to be one-thirtieth that of FBJ-LL cells. This motility of GD1a-expressing transfectants, which were produced by transfection of FBJ-LL cells with GM2/GD2 synthase cDNA, decreased with increases in their GD1a expression and HGF induced almost no motility in GD1a-pretreated FBJ-LL cells, indicating that GD1a inhibits the HGF-induced motility of GD1a; HGF; motility; scattering Gangliosides are sialylated glycosphingolipids found on the outer layer of the plasma membrane. Changes in ganglioside expression in cancer cells are strongly related to their metastatic potential. 1-5 Although increases in complex ganglioside expression in cancer cells have been considered to be associated with malignancy, in our previous study we found that the poorly metastatic FBJ-S1 cells highly expressed the complex ganglioside GD1a, whereas the highly metastatic FBJ-LL cells only slightly expressed this ganglioside. 6 GD1a inhibited the serum-induced motility of FBJ-LL cells and the metastatic potential of FBJ-LL cells was completely suppressed by enforced GD1a expression. 7 It is possible that GD1a suppresses metastasis of FBJ-LL cells by inhibiting cell migration. The target molecules of GD1a need to be identified to clarify the mechanism of inhibition of metastasis by GD1a. Key words:We recently found that HGF induces FBJ-LL cell motility 8 and that the serum-induced motility of FBJ-LL cells was decreased by treatment of the serum with anti-HGF antibody (unpublished data), suggesting that HGF is a migration-stimulating factor in serum. Since FBJ-LL cells metastasize to the liver and HGF is secreted by nonparenchymal liver cells, HGF may promote liver metastasis of FBJ-LL cells. We suspect that HGF may play a key role in FBJ-LL cell metastasis. HGF is a multipotential modulator of biologic activities in a variety of cell types and it influences the growth, motility, differentiation and morphogenesis of its target cells through the c-Met tyrosine kinase receptor. 9 HGF has been described as a potent chemotactic factor 10 and has been associated with the progression of carcinoma cells. 11 Overexpression of the HGF receptor, c-Met, in malignant cells has been reported in various tissues. 12 Hence HGF may play a crucial role in cancer metastasis.In the present study, we attempted to identify the target molecules of GD1a by analyzing the molecular mechanism of the inhibition of cell migration by GD1a. We found that GD1a inhibited the HGFinduced motility, morphologic change and formation of actin stress fibers in FBJ-LL cells through suppression of tyrosine phosphorylation ...

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Reduced cell migration, tumor growth and experimental metastasis of rat F-11 cells whose expression of GD3-synthase is suppressed

Zeng

Gao

2000

Int. J. Cancer

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We previously established a rat F‐11 cell line whose expression of ganglioside GD3 was inhibited by stable transfection of the anti‐sense vector against the GD3‐synthase gene, showing that specific inhibition of GD3‐synthase expression in tumor cells greatly reduced their growth rate in nude mice. Here, we report that down‐regulation of GD3‐synthase expression in anti‐sense–transfected F‐11 cells correlates with reduced cell migration and invasion in vitro and tumor growth and metastasis in vivo. When cultures were denuded of cells in a 1‐mm‐wide strip, the anti‐sense–transfected F‐11 cells migrated very slowly into the denuded area. Differences in migration between anti‐sense–transfected cells and control parental cells were easily apparent. In vitro invasion assay of F‐11 cells revealed a 3‐fold decrease in invasion ability from the GD3‐synthase–suppressed cells; colony formation in soft agar was not affected. Injection (i.v.) of control sense‐transfected and untransfected F‐11 cells resulted in multiple, large metastatic nodules in each of the 12 mice, whereas i.v. injection of anti‐sense–transfected F‐11 cells formed a single, small metastatic nodule in only 2 of the 8 nude mice. In addition, even if metastasis occurred, the anti‐sense–induced metastatic nodules were much smaller than the metastatic nodules formed by control F‐11 cells. These results demonstrate that suppression of GD3‐synthase expression, which results primarily in a marked decrease in the concentration of ganglioside GD3, greatly reduces cell spreading, invasion and both the incidence and growth rate of experimental metastasis of F‐11 cells. Int. J. Cancer 88:53–57, 2000. © 2000 Wiley‐Liss, Inc.

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Suppression by ganglioside GD1A of migration capability, adhesion to vitronectin and metastatic potential of highly metastatic FBJ-LL cells

Cited by 31 publications

References 17 publications

A Glycosphingolipid/Caveolin-1 Signaling Complex Inhibits Motility of Human Ovarian Carcinoma Cells

A Glycosphingolipid/Caveolin-1 Signaling Complex Inhibits Motility of Human Ovarian Carcinoma Cells

Ganglioside GD1a inhibits HGF-induced motility and scattering of cancer cells through suppression of tyrosine phosphorylation of c-Met

Reduced cell migration, tumor growth and experimental metastasis of rat F-11 cells whose expression of GD3-synthase is suppressed

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