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1.
Figure 1

Figure 1. From: Ganglioside GM3 Is Antiangiogenic in Malignant Brain Cancer.

Structure of Ganglioside GM3 (NeuAc-alpha 2→ 3Gal-beta1 → 4Glc-beta1 →1′ Ceramide) (from [14] with permission).

Thomas N. Seyfried, et al. J Oncol. 2010;2010:961243.
2.
Figure 2

Figure 2. From: Ganglioside GM3 Is Antiangiogenic in Malignant Brain Cancer.

Pathway for the synthesis of ganglioside GM2 from GM3 by GalNAc-T. GalNAc-T adds a beta-linked N-acetylgalactosamine residue to the galactose of GM3 to form GM2, a key step required for the synthesis of complex gangliosides, GM2, GM1, and GD1a. Antisense targeting of the GalNAc-T gene reduces GD1a content, while increasing GM3 content [7].

Thomas N. Seyfried, et al. J Oncol. 2010;2010:961243.
3.
Figure 7

Figure 7. From: Ganglioside GM3 Is Antiangiogenic in Malignant Brain Cancer.

GM3 inhibits the pro-angiogenic effects of GD1a in the in vivo Matrigel assay. Matrigel alone (control) or containing GD1a or GD1a with GM3 was injected subcutaneously (s.c.) in SCID mice as we described [49]. Plugs were photographed (12.5×) on day 7 after Matrigel injection.

Thomas N. Seyfried, et al. J Oncol. 2010;2010:961243.
4.
Figure 3

Figure 3. From: Ganglioside GM3 Is Antiangiogenic in Malignant Brain Cancer.

High-performance thin-layer chromatographic analysis of ganglioside distribution in the CT-2A astrocytoma: Control untransfected CT-2A (C), CT-2A transfected with empty vector alone (V), and CT-2A transfected with the antisense sequence to the GalNAc-T gene (T). Synthesized gangliosides appear as double bands due to ceramide structural heterogeneity. Analysis of synthesized gangliosides and standards (left lane) was as we described [7]. Knockdown of the GalNAc-T gene elevated GM3 content, while reducing GD1a content in the antisense T cells.

Thomas N. Seyfried, et al. J Oncol. 2010;2010:961243.
5.
Figure 8

Figure 8. From: Ganglioside GM3 Is Antiangiogenic in Malignant Brain Cancer.

GM3 inhibits VEGFR-2 and Akt phosphorylation in HUVEC. HUVECs were incubated with GM3 (100 ng/ml) in endothelial basal medium (EBM) for 24 hours and were then stimulated with VEGF (100 ng/ml) for 5 minutes as we described [49]. (a) Cell lysates were prepared and measurement of VEGFR-2 and Akt phosphorylation over total was analyzed using Western blots [49]. (b) VEGFR-2 and (c) Akt phosphorylation were significantly lower in GM3-treated HUVEC than in control HUVEC (P < .001). Values are expressed as means ± SEM (n = 3 independent experiments).

Thomas N. Seyfried, et al. J Oncol. 2010;2010:961243.
6.
Figure 6

Figure 6. From: Ganglioside GM3 Is Antiangiogenic in Malignant Brain Cancer.

GM3 reduces CT-2A tumor vascularity when added to the tumor microenvironment. Small fragments of the CT-2A tumor were grown in Matrigel that contained either no GM3 (control) or GM3 (40 μM). The tumor was grown in Matrigel for approximately two weeks in the flank of the syngeneic host C57BL/6 mice according to our standard procedures [7, 34]. Florid vascularization and the number and size thrombotic vessels were noticeably less in the presence than in the absence of GM3. Similar results were found in two independent experiments.

Thomas N. Seyfried, et al. J Oncol. 2010;2010:961243.
7.
Figure 5

Figure 5. From: Ganglioside GM3 Is Antiangiogenic in Malignant Brain Cancer.

Ganglioside shift reduces VEGF, HIF-1α, and NP-1 gene expression in CT-2A- cultured cells: Control untransfected CT-2A (C), CT-2A transfected with empty vector alone (V), and CT-2A transfected with the anti-sense sequence to (a) the GalNAc-T gene (T). VEGF (multiple splice variants: 400–600 bp), HIF-1α (365 bp), and NP-1 (551 bp) amplification products were detected in each tumor cell line. Experimental conditions are as we described [7]. The gene to β-actin levels are expressed as the means of three independent samples ± SE.*: Significant compared to control C and V cells at (b) the P < .01.

Thomas N. Seyfried, et al. J Oncol. 2010;2010:961243.
8.
Figure 4

Figure 4. From: Ganglioside GM3 Is Antiangiogenic in Malignant Brain Cancer.

Ganglioside shift reduces growth, VEGF gene and protein expression, and vascularity in the CT-2A astrocytoma: Control untransfected CT-2A (C), CT-2A transfected with empty vector alone (V), and CT-2A transfected with the antisense sequence to the GalNAc-T gene (T). (a) The values are expressed as mean mg wet weight ± SE.*: significant compared to control C and V tumors at the P < .01 level. CT-2A (n = 10), CT-2A/V (n = 12), and CT-2A/TNG (n = 14) independent tumors. (b) RT-PCR and Western blot for VEGF. Other details are in [7]. (c) Vascularity determined using factor VIII-immunostained microvessels per ×200 field (hpf, high-powered field) from tissue sections as we described [7].

Thomas N. Seyfried, et al. J Oncol. 2010;2010:961243.

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