Vascular endothelial cell growth factor (VEGF) produced by A-431 human epidermoid carcinoma cells and identification of VEGF membrane binding sites.

Myoken, Yoshinari; Kayada, Yoshiaki; Okamoto, Takashi; Kan, Mikio; Sato, Gordon; Sato, Jun

doi:10.1073/pnas.88.13.5819

Cited by 100 publications

(64 citation statements)

References 40 publications

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“…VEGF plays a crucial role in tumour angiogenesis and the inhibition of VEGF action decreases tumour growth in vivo (Kim et al, 1993;Goldman et al, 1998;Lin et al, 1998). Since the human A431 carcinoma cells secrete high amounts of VEGF (Myoken et al, 1991) and develop in nude mice tumours whose growth is highly VEGF-dependent (Melnyk et al, 1996), they provide a good model to test the availability of molecules that inhibit VEGF bioactivity. In this study, we assessed the anti-VEGF activity of CMDB7, described recently in vitro (Hamma-Kourbali et al, 2001), on A431 xenografted in nude mice, an extremely aggressive tumour model.…”

Section: Discussionmentioning

confidence: 99%

“…We have recently shown in vitro that it prevents the binding of VEGF 165 to human umbilical vein endothelial cell surface and thus inhibits VEGF 165 -induced phosphorylation of VEGFR-2 and consequently endothelial cell proliferation (Hamma-Kourbali et al, 2001). In the present study, we explored in vitro and in vivo the effects of CMDB7 on human epidermoid carcinoma A431 cells known to produce a high amount of VEGF and a minor quantity of bFGF (Myoken et al, 1991). The other peculiarity of A431 cells is the production of a newly identified splice form of VEGF, VEGF-162, which binds more efficiently than VEGF-165 to a natural basement membrane of endothelial cells (Lange et al, 2003).…”

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Carboxymethyl benzylamide dextran inhibits angiogenesis and growth of VEGF-overexpressing human epidermoid carcinoma xenograft in nude mice

et al. 2003

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Vascular endothelial growth factor (VEGF) expression is elevated in a wide variety of solid tumours. Inhibition of VEGF activities is able to reduce angiogenesis and tumour growth. We have recently shown in vitro that carboxymethyl dextran benzylamide (CMDB7) prevents the binding of VEGF 165 to its cell surface receptors and thus inhibits VEGF activities on endothelial cells. In the present study, we explored the effects of CMDB7 on highly aggressive human epidermoid carcinoma A431 cells known to overexpress epidermal growth factor receptors (EGFRs) and produce a high amount of VEGF and a minor quantity of bFGF. In vitro, CMDB7 blocked the mitogenic activity of A431-conditioned medium on endothelial cells. Concerning A431 cells, CMDB7 inhibited their proliferation and the VEGF 165 binding to them. In vivo, administration of CMDB7 (10 mg kg À1 ) three times per week for 2 weeks inhibited the growth of A431 xenografts in nude mice by 73% as compared to the control group. Immunostaining of endothelial cells with mouse-specific GSL-1 lectin in tumour sections revealed that CMDB7 also inhibited the density of intratumour endothelial cells by 66%. These findings demonstrate that CMDB7 has an efficient antiangiogenic and antitumour action in vivo even when tumour cells produce a high level of VEGF and EGFRs.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Carboxymethyl benzylamide dextran inhibits angiogenesis and growth of VEGF-overexpressing human epidermoid carcinoma xenograft in nude mice

et al. 2003

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“…A431 cells are known to secrete a large quantity of VEGF (Myoken et al, 1991), a potent angiogenic factor. We recently demonstrated that NaPaC interacted with VEGF 165 by forming a complex and inhibited the proliferation of endothelial cells stimulated by VEGF 165 (Di Benedetto et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…As we recently showed that NaPaC forms a complex with VEGF 165 (Di Benedetto et al, 2002) and as A431 cells secrete high amounts of VEGF 165 (Myoken et al, 1991) we tested, here, the effect of NaPaC on the binding of VEGF to A431 cells (Figure 3). Phenylacetate carboxymethyl benzylamide dextran inhibited the binding of VEGF 165 to A431 cells in a concentration-dependant manner with an IC 50 of 0.3 mM ( Figure 3A).…”

Section: Napac Inhibits the In Vitro Proliferation Of Epidermoid Carcmentioning

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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

et al. 2003

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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 ¼ 5 mM). Also, NaPaC decreased the binding of radiolabelled VEGF 165 to endothelial cells (IC 50 ¼ 0.2 mM). In vivo, we explored the effects of NaPaC (15 mg kg À1 ) 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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Expression of fibroblast growth factor-1 (FGF-1), FGF-2 and FGF receptor-1 in a human salivary-gland adenocarcinoma cell line: Evidence of autocrine growth

et al. 1996

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Fibroblast growth factor-I (FGF-I) and FGF-2 are heparinbinding polypeptides which express potent mitogenic properties in neoplastic cells. In the present study, we have examined the contribution of endogenous FGF-I and FGF-2 to the autocrine growth of HSY human salivary-gland adenocarcinoma cells in vitro. Using specific monoclonal antibodies against FGF-I and FGF-2, immunohistochemical analysis of HSY cells revealed strong expression of both FGF-I and FGF-2 in the cytoplasm and nucleus. Consistent with these data, 2 molecular mass species of pM FCF-2-specific anti-sense oligonucleotides resulted in a 76% inhibition. These effects were dose-dependent and specific, since sense oligonucleotides were ineffective in inhibiting HSY cell growth at the same concentration. Furthermore, HSY cell growth was suppressed in the presence of anti-FGF-I or anti-FGF-2 neutralizing antibody, resulting in a 58% inhibition at 8 pmg/ml. Our observations suggest that FGF-I and FGF-2 may act as autocrine regulatom by interacting with FGF recept o n on HSY cells. o 1996 Wiley-Liss, Inc.

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Vascular endothelial cell growth factor (VEGF) produced by A-431 human epidermoid carcinoma cells and identification of VEGF membrane binding sites.

Cited by 100 publications

References 40 publications

Carboxymethyl benzylamide dextran inhibits angiogenesis and growth of VEGF-overexpressing human epidermoid carcinoma xenograft in nude mice

Carboxymethyl benzylamide dextran inhibits angiogenesis and growth of VEGF-overexpressing human epidermoid carcinoma xenograft in nude mice

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

Expression of fibroblast growth factor-1 (FGF-1), FGF-2 and FGF receptor-1 in a human salivary-gland adenocarcinoma cell line: Evidence of autocrine growth

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