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Ganglioside GD3 induces convergence and synergism of adhesion and hepatocyte growth factor/Met signals in melanomas.

Furukawa K, Kambe M, Miyata M, Ohkawa Y, Tajima O, Furukawa K - Cancer Sci. (2013)

Bottom Line: In this study, we analyzed the effects of GD3 expression on cell signals triggered by hepatocyte growth factor (HGF)/Met interaction and by adhesion to collagen type I (CL-I).When resistance to induced apoptosis by H2O2 was examined, only GD3+ cells treated with both HGF and adhesion to CL-I showed clearly low percentages of dead cells compared with GD3- cells or GD3+ cells treated with either one of the stimulants.Cell growth measured by 5-ethynyl-2' deoxyuridine uptake also showed synergistic effects in GD3+ cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai, Japan; Department of Biochemistry II, Nagoya University Graduate School of Medicine, Nagoya, Japan.

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Convergence of signaling molecules in the vicinity of membranes and synergistic enhancement of the signaling and phenotypes in ganglioside GD3+ N1 cells. (A) Phosphatidylinositol-3-OH kinase (PI3K)–Akt exists downstream of the collagen type I (CL-I)/integrin-mediated signaling and hepatocyte growth factor (HGF)/Met-mediated signaling pathway. After adhesion of cells to CL-I, focal adhesion kinase (FAK) is phosphorylated (P), leading to activation of PI3K and subsequent Akt phosphorylation. After binding of hepatocyte growth factor (HGF), Met is phosphorylated and growth factor receptor bound protein-1 (Grb-1) can bind to phosphorylated Met, then PI3K is activated resulting in Akt phosphorylation. (B) Ras-Erks exist downstream of the CL-I/integrin-mediated signaling pathway. After adhesion of cells to CL-I, FAK is phosphorylated and an Src family kinase, Yes, binds phosphorylated FAK, then sequential activation of the signaling pathway takes place. After binding of HGF, Met is phosphorylated and Grb2–Sos can bind to phosphorylated Met, resulting in the activation of Ras, then of Erks. CL type I, collagen type I; PI(3,4)P2, phosphatidylinositol 3,4-bisphosphate; PI(4)P, phosphatidylinositol 4-monophosphate.
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fig09: Convergence of signaling molecules in the vicinity of membranes and synergistic enhancement of the signaling and phenotypes in ganglioside GD3+ N1 cells. (A) Phosphatidylinositol-3-OH kinase (PI3K)–Akt exists downstream of the collagen type I (CL-I)/integrin-mediated signaling and hepatocyte growth factor (HGF)/Met-mediated signaling pathway. After adhesion of cells to CL-I, focal adhesion kinase (FAK) is phosphorylated (P), leading to activation of PI3K and subsequent Akt phosphorylation. After binding of hepatocyte growth factor (HGF), Met is phosphorylated and growth factor receptor bound protein-1 (Grb-1) can bind to phosphorylated Met, then PI3K is activated resulting in Akt phosphorylation. (B) Ras-Erks exist downstream of the CL-I/integrin-mediated signaling pathway. After adhesion of cells to CL-I, FAK is phosphorylated and an Src family kinase, Yes, binds phosphorylated FAK, then sequential activation of the signaling pathway takes place. After binding of HGF, Met is phosphorylated and Grb2–Sos can bind to phosphorylated Met, resulting in the activation of Ras, then of Erks. CL type I, collagen type I; PI(3,4)P2, phosphatidylinositol 3,4-bisphosphate; PI(4)P, phosphatidylinositol 4-monophosphate.

Mentions: These results are summarized in a schema in Figure9.


Ganglioside GD3 induces convergence and synergism of adhesion and hepatocyte growth factor/Met signals in melanomas.

Furukawa K, Kambe M, Miyata M, Ohkawa Y, Tajima O, Furukawa K - Cancer Sci. (2013)

Convergence of signaling molecules in the vicinity of membranes and synergistic enhancement of the signaling and phenotypes in ganglioside GD3+ N1 cells. (A) Phosphatidylinositol-3-OH kinase (PI3K)–Akt exists downstream of the collagen type I (CL-I)/integrin-mediated signaling and hepatocyte growth factor (HGF)/Met-mediated signaling pathway. After adhesion of cells to CL-I, focal adhesion kinase (FAK) is phosphorylated (P), leading to activation of PI3K and subsequent Akt phosphorylation. After binding of hepatocyte growth factor (HGF), Met is phosphorylated and growth factor receptor bound protein-1 (Grb-1) can bind to phosphorylated Met, then PI3K is activated resulting in Akt phosphorylation. (B) Ras-Erks exist downstream of the CL-I/integrin-mediated signaling pathway. After adhesion of cells to CL-I, FAK is phosphorylated and an Src family kinase, Yes, binds phosphorylated FAK, then sequential activation of the signaling pathway takes place. After binding of HGF, Met is phosphorylated and Grb2–Sos can bind to phosphorylated Met, resulting in the activation of Ras, then of Erks. CL type I, collagen type I; PI(3,4)P2, phosphatidylinositol 3,4-bisphosphate; PI(4)P, phosphatidylinositol 4-monophosphate.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4317880&req=5

fig09: Convergence of signaling molecules in the vicinity of membranes and synergistic enhancement of the signaling and phenotypes in ganglioside GD3+ N1 cells. (A) Phosphatidylinositol-3-OH kinase (PI3K)–Akt exists downstream of the collagen type I (CL-I)/integrin-mediated signaling and hepatocyte growth factor (HGF)/Met-mediated signaling pathway. After adhesion of cells to CL-I, focal adhesion kinase (FAK) is phosphorylated (P), leading to activation of PI3K and subsequent Akt phosphorylation. After binding of hepatocyte growth factor (HGF), Met is phosphorylated and growth factor receptor bound protein-1 (Grb-1) can bind to phosphorylated Met, then PI3K is activated resulting in Akt phosphorylation. (B) Ras-Erks exist downstream of the CL-I/integrin-mediated signaling pathway. After adhesion of cells to CL-I, FAK is phosphorylated and an Src family kinase, Yes, binds phosphorylated FAK, then sequential activation of the signaling pathway takes place. After binding of HGF, Met is phosphorylated and Grb2–Sos can bind to phosphorylated Met, resulting in the activation of Ras, then of Erks. CL type I, collagen type I; PI(3,4)P2, phosphatidylinositol 3,4-bisphosphate; PI(4)P, phosphatidylinositol 4-monophosphate.
Mentions: These results are summarized in a schema in Figure9.

Bottom Line: In this study, we analyzed the effects of GD3 expression on cell signals triggered by hepatocyte growth factor (HGF)/Met interaction and by adhesion to collagen type I (CL-I).When resistance to induced apoptosis by H2O2 was examined, only GD3+ cells treated with both HGF and adhesion to CL-I showed clearly low percentages of dead cells compared with GD3- cells or GD3+ cells treated with either one of the stimulants.Cell growth measured by 5-ethynyl-2' deoxyuridine uptake also showed synergistic effects in GD3+ cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomedical Sciences, Chubu University College of Life and Health Sciences, Kasugai, Japan; Department of Biochemistry II, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Show MeSH
Related in: MedlinePlus