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      Phytochemicals Targeting VEGF and VEGF-Related Multifactors as Anticancer Therapy

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          Abstract

          The role of vascular endothelial growth factor (VEGF) in cancer cells is not limited to angiogenesis; there are also multiple factors, such as neuropilins (non-tyrosine kinases receptors), tyrosine kinases receptors, immunodeficiencies, and integrins, that interact with VEGF signaling and cause cancer initiation. By combating these factors, tumor progression can be inhibited or limited. Natural products are sources of several bioactive phytochemicals that can interact with VEGF-promoting factors and inhibit them through various signaling pathways, thereby inhibiting cancer growth. This review provides a deeper understanding of the relation and interaction of VEGF with cancer-promoting factors and phytochemicals in order to develop multi-targeted cancer prevention and treatment.

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          Signal transduction by vascular endothelial growth factor receptors.

          Sina Koch, Sònia Tugues, Xiujuan Li … (2011)
          VEGFs (vascular endothelial growth factors) control vascular development during embryogenesis and the function of blood vessels and lymphatic vessels in the adult. There are five related mammalian ligands, which act through three receptor tyrosine kinases. Signalling is modulated through neuropilins, which act as VEGF co-receptors. Heparan sulfate and integrins are also important modulators of VEGF signalling. Therapeutic agents that interfere with VEGF signalling have been developed with the aim of decreasing angiogenesis in diseases that involve tissue growth and inflammation, such as cancer. The present review will outline the current understanding and consequent biology of VEGF receptor signalling.
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            Bevacizumab (Avastin), a humanized anti-VEGF monoclonal antibody for cancer therapy.

            Napoleone Ferrara, Kenneth J Hillan, William E Novotny (2005)
            Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen in vitro and an angiogenic inducer in vivo. The tyrosine kinases Flt-1 (VEGFR-1) and Flk-1/KDR (VEGFR-2) are high affinity VEGF receptors. VEGF plays an essential role in developmental angiogenesis and is important also for reproductive and bone angiogenesis. Substantial evidence also implicates VEGF as a mediator of pathological angiogenesis. Anti-VEGF monoclonal antibodies and other VEGF inhibitors block the growth of several tumor cell lines in nude mice. Clinical trials with VEGF inhibitors in a variety of malignancies are ongoing. Recently, a humanized anti-VEGF monoclonal antibody (bevacizumab; Avastin) has been approved by the FDA as a first-line treatment for metastatic colorectal cancer in combination with chemotherapy. Furthermore, VEGF is implicated in intraocular neovascularization associated with diabetic retinopathy and age-related macular degeneration.
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              Integrin alpha 6 regulates glioblastoma stem cells.

              Justin D. Lathia, Joseph Gallagher, John M. Heddleston … (2010)
              Cancer stem cells (CSCs) are a subpopulation of tumor cells suggested to be critical for tumor maintenance, metastasis, and therapeutic resistance. Prospective identification and targeting of CSCs are therefore priorities for the development of novel therapeutic paradigms. Although CSC enrichment has been achieved with cell surface proteins including CD133 (Prominin-1), the roles of current CSC markers in tumor maintenance remain unclear. We examined the glioblastoma stem cell (GSC) perivascular microenvironment in patient specimens to identify enrichment markers with a functional significance and identified integrin alpha6 as a candidate. Integrin alpha6 is coexpressed with conventional GSC markers and enriches for GSCs. Targeting integrin alpha6 in GSCs inhibits self-renewal, proliferation, and tumor formation capacity. Our results provide evidence that GSCs express high levels of integrin alpha6, which can serve not only as an enrichment marker but also as a promising antiglioblastoma therapy.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Clin Med
                Journal ID (iso-abbrev): J Clin Med
                Journal ID (publisher-id): jcm
                Title: Journal of Clinical Medicine
                Publisher: MDPI
                ISSN (Electronic): 2077-0383
                Publication date (Electronic): 12 March 2019
                Publication date Collection: March 2019
                Volume: 8
                Issue: 3
                Electronic Location Identifier: 350
                Affiliations
                [1 ]Department of Pharmacognosy, Faculty of Pharmaceutical Science, Government College University, Faisalabad, Faisalabad 38000, Pakistan
                [2 ]College of Pharmacy, Gachon University, No. 191, Hambakmoero, Yeonsu-gu, Incheon 21936, Korea; subedilali@ 123456gmail.com (L.S.); ettienne1226@ 123456gmail.com (H.W.K.); zahra.khan37@ 123456gmail.com (Z.K.)
                [3 ]Institute of Environmental Sciences and Engineering, School of Civil and Environmental Engineering, National University of Sciences and Technology, Sector H-12, Islamabad 44000, Pakistan; zahra@ 123456iese.nust.edu.pk
                [4 ]School of Agriculture and Environment, The University of Western Australia, Perth, WA 6009, Australia; mqfarooqi@ 123456gmail.com
                [5 ]Gachon Institute of Pharmaceutical Science, Gachon University, No. 191 Hambakmoe-ro, Yeonsu-gu, Incheon 21936, Korea
                Author notes
                [* ]Correspondence: amnaparvin@ 123456gmail.com (A.P.); sunnykim@ 123456gachon.ac.kr (S.Y.K.); Tel.: +82-10-5925-2733 (A.P.); +82-10-2292-9232 (S.Y.K.)
                [†]

                All these authors equally contributed to this work.

                Author information
                https://orcid.org/0000-0003-4851-7650
                https://orcid.org/0000-0003-4918-9791
                https://orcid.org/0000-0001-8044-5613
                Article
                Publisher ID: jcm-08-00350
                DOI: 10.3390/jcm8030350
                PMC ID: 6462934
                PubMed ID: 30871059
                SO-VID: 873c7a11-9ae4-47ff-abf7-181c32adbc21
                Copyright © © 2019 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 30 January 2019
                Date accepted : 06 March 2019
                Categories
                Subject: Review

                Keywords: vascular endothelial growth factor,receptor tyrosine kinases,neuropilins,epithelial–mesenchymal transition,hypoxia-inducible factor,estrogen receptor-β,prolyl hydroxylase 2,notch ligand delta-like 4,focal adhesion kinases,placental growth factor-1
                Data availability:
                Keywords: vascular endothelial growth factor, receptor tyrosine kinases, neuropilins, epithelial–mesenchymal transition, hypoxia-inducible factor, estrogen receptor-β, prolyl hydroxylase 2, notch ligand delta-like 4, focal adhesion kinases, placental growth factor-1

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