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Vascular Endothelial Cell Growth Factor (VEGF), An Emerging Target for Cancer Chemotherapy
Abstract
Angiogenesis is a process of development and of growth of new capillary blood vessels from pre-existing vessels. When pathological, it contributes to the development of numerous types of tumors, and the formation of metastases. In order to grow, carcinoma need new blood vessels to form so that they can feed themselves. Therefore, nowadays the concept according to which the development of cancer is angiogenesis dependent is generally recognized. This concept makes the control of tumoral angiogenesis one of the promising therapeutic ways in cancerology. The transition from the latent phase to the invasive and metastatic phase of a cancer is linked to what is called the angiogenic switch. It implies complex cellular and molecular interactions between cancerous cells, endothelial cells and the components of the extra-cellular matrix and namely the existence of specific proteins secreted by the tumoral cells able to stimulate the proliferation of capillary endothelial cells. Among them, VEGF, Vascular Endothelial Growth Factor was found in several types of tumors. It has shown a tumoral angiogenic activity in vitro and in vivo, and thus is a privileged target for the control of angiogenesis in an anti-tumoral goal. The role of VEGF in tumoral angiogenesis has been extensively studied. It has been proved to undergo as well autocrine as paracrine stimulation of tumoral angiogenesis. During the last few years, several members of the VEGF family have been described namely the VEGF-A, B, C, D, E and placenta growth factor (PlGF) among which VEGF-A (121 aminoacids) plays a role of prime importance in angiogenesis. VEGF is a 45 kDA glycoprotein, homodimeric, basic, and able to bind heparin. The three-dimensional structure of VEGF has been recently determined, by X-rays diffraction, and NMR spectroscopy. The different forms of the VEGF bind to receptors that exhibit a tyrosine-kinase activity (RTK). The specific action of the VEGF on the endothelial cells is mainly regulated by two types of RTK of the VEGF family, VEGFR1, or Flt-1, and VEGFR2, or KDR/Flk-1. Mutagenesis studies have shown that only a small number of VEGF residues are important and essential for the binding with RTK. Data described to date from the studies of VEGF/RTK interactions agree to the hypothesis that KDR receptor is the main human receptor responsible for the VEGF activity in both physiological and pathological vascular development, and VEGF-KDR signalling pathway has been validated as a priority target for the development of anti- and pro- angiogenic agents. Therefore angiogenesis mediated by VEGF constitutes a new target for anti-cancer therapy which has explored through different ways of intervention aiming at the blocking of the tumoral angiogenesis. The main ones are: -Struggle against the stroma degradation and invasion by the neo-vessels -Inhibition of activated endothelial cells. -Inhibition of angiogenic factors production and of their receptors. -Inhibition of the VEGF signal pathway, by peptides blocking the bond between VEGF and its receptors through the inhibition of intracellular transduction of VEGF signal. In conclusion, this bibliographic study allows to situate works of medicinal chemistry in the context of present knowledge concerning the vascular endothelial growth factor (VEGF) and its role in angiogenesis.
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“In patients being treated for malignancies, antineoplastic drugs that target the VEGF (vascular endothelial growth factor) pathway have emerged as inducers of hypertension.225–227”
From Resistant Hypertension: Detection, Evaluation, and Management: A Scientific Statement From the American Heart Association (2018) · cites this paper as [227]
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“VEGF presented a median score of 190 (180-255); MMP-2 presented a median score of 55 (6-204), with 14 (15.”
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“Vascular endothelial growth factor strongly induces angiogenesis and increases permeability of blood vessels.(15) Vascular endothelial growth factor and its receptors are expressed in both the endometrium and trophoblast cells,(16) suggesting that VEGF/VEGF receptor (VEGFR)-2 signaling might be critical in placental a…”
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Metadata
- Authors
- Shinkaruk, S., Bayle, M., Lain, G., & Deleris, G.
- Affiliations
- Inserm (FR)
- ORCID
- Shinkaruk, S.
- Venue
- Current Medicinal Chemistry-Anti-Cancer Agents
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2003-03-01
- Volume
- 3
- Issue
- 2
- Pages
- 95-117
- ISSN
- 1568-0118 (ISSN-L)
- OpenAlex
- W2070230256
- Cited by
- 219
- References
- 0
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 5 · 2023: 6 · 2022: 2 · 2021: 2 · 2020: 5 · 2019: 8 · 2018: 14 · 2017: 12 · 2016: 11 · 2015: 13 · 2014: 15 · 2013: 10 · 2012: 11
- FWCI
- 3.68
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Anti-Cancer Agents in Medicinal Chemistry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Oncology › Lymphatic System and Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Mechanisms and Therapy
- Keywords
- vascular endothelial growth factor, angiogenesis, tumor angiogenesis, anti-angiogenic cancer therapy, VEGF receptors, VEGFR2, VEGFR1, VEGF-A, VEGF family, angiogenic switch, metastasis, autocrine and paracrine signaling, receptor tyrosine kinase, anti-VEGF therapy, VEGF inhibitors
- MeSH terms
- Animals, Endothelium, Vascular, Humans, Lymphokines, Neoplasm Metastasis, Neoplasms, Neovascularization, Pathologic, Endothelial Growth Factors, Paracrine Communication, Angiogenesis Inhibitors, Intercellular Signaling Peptides and Proteins, Receptors, Vascular Endothelial Growth Factor, Vascular Endothelial Growth Factors, Vascular Endothelial Growth Factor A
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