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Inhibition of epidermoid carcinoma A431 cell growth and angiogenesis in nude mice by early and late treatment with a novel dextran derivative.

Di Benedetto M, Starzec A, Vassy R, Perret GY, Crépin M, Kraemer M - Br. J. Cancer (2003)

Bottom Line: Also, NaPaC decreased the binding of radiolabelled VEGF(165) to endothelial cells (IC(50)=0.2 micro M).In contrast, vessel area was decreased only when NaPaC was injected early (35%).These results show that NaPaC has a potent inhibitory effect, dependent on treatment outset, on epidermoid carcinoma growth associated with an intratumour microvascular network diminution and an aponecrosis increase.

View Article: PubMed Central - PubMed

Affiliation: Laboratoire d'Oncologie Cellulaire et Moléculaire, UPRES 2360, Université Paris 13, 74 rue Marcel Cachin, 93017 Bobigny cedex, France. melanie.dibenedetto@ibl.fr

ABSTRACT
We investigated the effect of a new dextran derivative, phenylacetate carboxymethyl benzylamide dextran (NaPaC), on epidermoid carcinoma A431 cells secreting a large quantity of angiogenic factor, vascular endothelial growth factor (VEGF). In vitro, NaPaC inhibited the proliferation of A431 cells (IC(50)=5 micro M). Also, NaPaC decreased the binding of radiolabelled VEGF(165) to endothelial cells (IC(50)=0.2 micro M). In vivo, we explored the effects of NaPaC (15 mg kg(-1)) on A431 xenograft growth starting the drug administration at the time of tumour cell inoculation (early treatment) and 1 week later, when tumours were well established (late treatment). Early treatment was more efficient on tumour inhibition (70% vs control) than late treatment (50% vs control). Early and late NaPaC-treatment increased the aponecrosis in tumour by 70 and 30%, respectively. Whatever treatment, NaPaC inhibited the intratumour endothelial cell density in the same manner. In contrast, vessel area was decreased only when NaPaC was injected early (35%). These results show that NaPaC has a potent inhibitory effect, dependent on treatment outset, on epidermoid carcinoma growth associated with an intratumour microvascular network diminution and an aponecrosis increase. As this drug is nontoxic at efficient dose, it offers interesting perspectives for the therapy of malignant lesions.

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Related in: MedlinePlus

NaPaC inhibits the VEGF165 binding to HUV-EC endothelial cells. Cells were incubated with a fixed concentration of [125I]VEGF165 (7 pM) in the absence or presence of NaPaC at various concentrations (0.01–24 μM)
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fig4: NaPaC inhibits the VEGF165 binding to HUV-EC endothelial cells. Cells were incubated with a fixed concentration of [125I]VEGF165 (7 pM) in the absence or presence of NaPaC at various concentrations (0.01–24 μM)

Mentions: Phenylacetate carboxymethyl benzylamide dextran inhibited the binding of VEGF165 to human umbilical vein endothelial cells (HUV-EC) in a concentration-dependant manner with an IC50 of 0.2 μM (Figure 4Figure 4


Inhibition of epidermoid carcinoma A431 cell growth and angiogenesis in nude mice by early and late treatment with a novel dextran derivative.

Di Benedetto M, Starzec A, Vassy R, Perret GY, Crépin M, Kraemer M - Br. J. Cancer (2003)

NaPaC inhibits the VEGF165 binding to HUV-EC endothelial cells. Cells were incubated with a fixed concentration of [125I]VEGF165 (7 pM) in the absence or presence of NaPaC at various concentrations (0.01–24 μM)
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2741107&req=5

fig4: NaPaC inhibits the VEGF165 binding to HUV-EC endothelial cells. Cells were incubated with a fixed concentration of [125I]VEGF165 (7 pM) in the absence or presence of NaPaC at various concentrations (0.01–24 μM)
Mentions: Phenylacetate carboxymethyl benzylamide dextran inhibited the binding of VEGF165 to human umbilical vein endothelial cells (HUV-EC) in a concentration-dependant manner with an IC50 of 0.2 μM (Figure 4Figure 4

Bottom Line: Also, NaPaC decreased the binding of radiolabelled VEGF(165) to endothelial cells (IC(50)=0.2 micro M).In contrast, vessel area was decreased only when NaPaC was injected early (35%).These results show that NaPaC has a potent inhibitory effect, dependent on treatment outset, on epidermoid carcinoma growth associated with an intratumour microvascular network diminution and an aponecrosis increase.

View Article: PubMed Central - PubMed

Affiliation: Laboratoire d'Oncologie Cellulaire et Moléculaire, UPRES 2360, Université Paris 13, 74 rue Marcel Cachin, 93017 Bobigny cedex, France. melanie.dibenedetto@ibl.fr

ABSTRACT
We investigated the effect of a new dextran derivative, phenylacetate carboxymethyl benzylamide dextran (NaPaC), on epidermoid carcinoma A431 cells secreting a large quantity of angiogenic factor, vascular endothelial growth factor (VEGF). In vitro, NaPaC inhibited the proliferation of A431 cells (IC(50)=5 micro M). Also, NaPaC decreased the binding of radiolabelled VEGF(165) to endothelial cells (IC(50)=0.2 micro M). In vivo, we explored the effects of NaPaC (15 mg kg(-1)) on A431 xenograft growth starting the drug administration at the time of tumour cell inoculation (early treatment) and 1 week later, when tumours were well established (late treatment). Early treatment was more efficient on tumour inhibition (70% vs control) than late treatment (50% vs control). Early and late NaPaC-treatment increased the aponecrosis in tumour by 70 and 30%, respectively. Whatever treatment, NaPaC inhibited the intratumour endothelial cell density in the same manner. In contrast, vessel area was decreased only when NaPaC was injected early (35%). These results show that NaPaC has a potent inhibitory effect, dependent on treatment outset, on epidermoid carcinoma growth associated with an intratumour microvascular network diminution and an aponecrosis increase. As this drug is nontoxic at efficient dose, it offers interesting perspectives for the therapy of malignant lesions.

Show MeSH
Related in: MedlinePlus