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Molecular Mechanisms of Angiogenesis and Cancer
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Molecular Mechanisms of Angiogenesis and Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 January 2025 | Viewed by 6627

Special Issue Editor

Dr. Vijay Avin

E-Mail Website
Guest Editor
Department of Pharmacology and Regenerative Medicine, University of Illinois at Chicago, Chicago, IL, USA
Interests: vascular biology; endothelial cell signalling; tumor angiogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The primitive network of blood vessels generated during vasculogenesis, expands by intussusception into the tumor microenvironment to nurture the tumor cells and metastasis to the different organs. We now know there are various molecular players involved in tumor angiogenesis but, the sequential and spatial expression of pro-angiogenic molecular players are not as well coordinated in tumors as in physiological angiogenesis, and their mechanism of action is poorly understood. Despite the consequences of the mechanism involved, the manifestation of cancer cells in tumor vessels has significant implications for metastasis of cancer cells to various organs and for the design of anti-angiogenic therapy. It is an open question to comprehend the molecular basis of angiogenic vessels result from cancer cells invading the vessel lumen or from cancer cells mocking endothelial cells or from co-opted vessels or from the apoptosis of endothelial cells which exposes underlying cancer cells.

The aim of this special issue entitled “Molecular Mechanism of Angiogenesis and Cancer” will be the blend of translational science and basic science emphasizing on the molecular basis of tumor angiogenesis and molecular signaling network required for anti-angiogenic therapy. Great contemplations will be given to the original research articles of identifying novel molecular mechanisms, studies showing new molecular targets and their signaling during angiogenesis, and identification of new targetable therapeutic agents and their molecular mechanisms on improving prognosis. The review of literature highlighting the current knowledge of angiogenesis and cancer are also welcome.

Dr. Vijay Avin
Guest Editor

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • angiogenesis
  • cancer
  • tumor angiogenesis
  • VEGF signaling
  • VEGFR2
  • HIF1a
  • transcription factors
  • anti-angiogenesis
  • anti-angiogenic therapy
  • angiogenesis inhibitors
  • endothelia cells
  • tumor associated Endothelial cells
  • metastasis
  • hypoxia
  • cancer differentiation
  • cancer stem cells
  • endothelial cell differentiation

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Published Papers (3 papers)

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Research

9 pages, 1440 KiB  
Communication
Lack of VEGFA/KDR Signaling in Conventional Renal Cell Carcinoma Explains the Low Efficacy of Target Therapy and Frequent Adverse Events
by Lehel Peterfi, Maria V. Yusenko, Gyula Kovacs and Tamas Beothe
Int. J. Mol. Sci. 2024, 25(13), 7359; https://doi.org/10.3390/ijms25137359 - 4 Jul 2024
Viewed by 917
Abstract
It is acknowledged that conventional renal cell carcinoma (cRCC), which makes up 85% of renal malignancies, is a highly vascular tumor. Humanized monoclonal antibodies were developed to inhibit tumor neo-angiogenesis, which is driven by VEGFA/KDR signaling. The results largely met our expectations, and [...] Read more.
It is acknowledged that conventional renal cell carcinoma (cRCC), which makes up 85% of renal malignancies, is a highly vascular tumor. Humanized monoclonal antibodies were developed to inhibit tumor neo-angiogenesis, which is driven by VEGFA/KDR signaling. The results largely met our expectations, and in several cases, adverse events occurred. Our study aimed to analyze the expression of VEGFA and its receptor KDR by immunohistochemistry in tissue multi-array containing 811 cRCC and find a correlation between VEGFA/KDR signaling and new vessel formation. None of the 811 cRCC displayed VEGFA-positive immunostaining. However, each glomerulus in normal kidney showed VEGFA-positive endothelial cells. KDR expression in endothelial meshwork was found in only 9% of cRCC, whereas 2% of the cRCC displayed positive KDR reaction in the cytoplasm of tumor cells. Our results disclose the involvement of VEGFA/KDR signaling in the neo-vascularization of cRCC and explain the frequent resistance to drugs targeting the VEGFA/KDR signaling and the high frequency of adverse events. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Angiogenesis and Cancer)
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12 pages, 2690 KiB  
Article
THBS1 and THBS2 Enhance the In Vitro Proliferation, Adhesion, Migration and Invasion of Intrahepatic Cholangiocarcinoma Cells
by Eleonora Corbella, Claudia Fara, Francesca Covarelli, Veronica Porreca, Biagio Palmisano, Giuseppina Mignogna, Alessandro Corsi, Mara Riminucci, Bruno Maras and Carmine Mancone
Int. J. Mol. Sci. 2024, 25(3), 1782; https://doi.org/10.3390/ijms25031782 - 1 Feb 2024
Cited by 2 | Viewed by 1981
Abstract
In intrahepatic cholangiocarcinoma (iCCA), thrombospondin 1 (THBS1) and 2 (THBS2) are soluble mediators released in the tumor microenvironment (TME) that contribute to the metastatic spreading of iCCA cells via a lymphatic network by the trans-differentiation of vascular endothelial cells to a lymphatic-like phenotype. [...] Read more.
In intrahepatic cholangiocarcinoma (iCCA), thrombospondin 1 (THBS1) and 2 (THBS2) are soluble mediators released in the tumor microenvironment (TME) that contribute to the metastatic spreading of iCCA cells via a lymphatic network by the trans-differentiation of vascular endothelial cells to a lymphatic-like phenotype. To study the direct role of THBS1 and THBS2 on the iCCA cells, well-established epithelial (HuCCT-1) and mesenchymal (CCLP1) iCCA cell lines were subjected to recombinant human THBS1 and THBS2 (rhTHBS1, rhTHBS2) for cellular function assays. Cell growth, cell adhesion, migration, and invasion were all enhanced in both CCLP1 and HuCCT-1 cells by the treatment with either rhTHBS1 or rhTHBS2, although they showed some variability in their intensity of speeding up cellular processes. rhTHBS2 was more intense in inducing invasiveness and in committing the HuCCT-1 cells to a mesenchymal-like phenotype and was therefore a stronger enhancer of the malignant behavior of iCCA cells compared to rhTHBS1. Our data extend the role of THBS1 and THBS2, which are not only able to hinder the vascular network and promote tumor-associated lymphangiogenesis but also exacerbate the malignant behavior of the iCCA cells. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Angiogenesis and Cancer)
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14 pages, 2222 KiB  
Article
Resveratrol, an Inhibitor Binding to VEGF, Restores the Pathology of Abnormal Angiogenesis in Retinopathy of Prematurity (ROP) in Mice: Application by Intravitreal and Topical Instillation
by Wei-Hui Hu, Xiao-Yong Zhang, Ka-Wing Leung, Ran Duan, Ting-Xia (Tina) Dong, Qi-Wei Qin and Karl Wah-Keung Tsim
Int. J. Mol. Sci. 2022, 23(12), 6455; https://doi.org/10.3390/ijms23126455 - 9 Jun 2022
Cited by 4 | Viewed by 2524
Abstract
Retinopathy of prematurity (ROP) is a severe eye disease leading to blindness. Abnormal vessel formation is the pathological hallmark of neovascular ROP. In forming vessels, vascular endothelial growth factor (VEGF) is an important stimulator. The current anti-ROP therapy has focused on bevacizumab, a [...] Read more.
Retinopathy of prematurity (ROP) is a severe eye disease leading to blindness. Abnormal vessel formation is the pathological hallmark of neovascular ROP. In forming vessels, vascular endothelial growth factor (VEGF) is an important stimulator. The current anti-ROP therapy has focused on bevacizumab, a monoclonal antibody against VEGF, and pazopanib, a tyrosine kinase inhibitor on the VEGF receptor (VEGFR). Several lines of evidence have proposed that natural compounds may be more effective and safer for anti-VEGF function. Resveratrol, a common natural compound, binds to VEGF and blocks its interaction with VEGFR, thereafter suppressing angiogenesis. Here, we evaluate the efficacy of intravitreal injection, or topical instillation (eye drops), of resveratrol into the eyes of mice suffering from oxygen-induced retinopathy, i.e., developing ROP. The treatment of resveratrol significantly relieved the degree of vascular distortion, permeability and hyperplasia; the efficacy could be revealed by both methods of resveratrol application. In parallel, the treatments of resveratrol inhibited the retinal expressions of VEGF, VEGFR and CD31. Moreover, the applied resveratrol significantly relieved the damage caused by oxygen radicals through upregulating the level of superoxide dismutase (SOD) and downregulating the level of malondialdehyde (MDA) in the retina. Taken together, the potential therapeutic benefit of resveratrol in pro-angiogenic diseases, including retinopathy, can be considered. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Angiogenesis and Cancer)
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