Angiogenesis in Cancer Therapy

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell and Gene Therapy".

Deadline for manuscript submissions: closed (30 June 2020) | Viewed by 3224

Special Issue Editors


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Guest Editor
Department of Molecular Cardiology, Joseph J. Jacobs Center for Thrombosis and Vascular Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA
Interests: angiogenesis; endothelial cells; integrins; extracellular matrix; cell adhesion; tumor progression; vascular biology; signal transduction in endothelium and platelets; oxidative stress and vasculature; toll-like receptors in angiogenesis

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Guest Editor
Department of Neuroscience, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44106, USA
Interests: angiogenesis; tumor angiogenesis; innate immunity of vasculature; toll-like receptors in angiogenesis; endothelial cells; extracellular matrix; endothelial mechanosensing

Special Issue Information

Dear Colleagues,

As human longevity continues to increase and a significant portion (>25%) of the world population is already aged over 50, neoplasm incident rates are expected to climb and pose a significant public health and economic burden. While it is already well established that tumors must acquire pro-angiogenic properties in order to facilitate growth and metastasize, exciting new research is linking interplay between tumor growth, vascular biology, and immunology. It is becoming evident that not only is the immune system capable of either suppressing or promoting tumor growth, but it is also capable of modulating the endothelium in order to achieve these results. Indeed, both anti-angiogenics and immunotherapies have had variable successes in clinical trials. As a result, studies that seek to elucidate interactions between the immune system and the endothelium in the context of the tumor microenvironment are of considerable interest to the future of disease treatment. However, current underpinnings of myeloid cell–endothelial cell interactions that promote disease remain poorly defined.

This Special Issue aims to summarize the current knowledge of the role of the immune system in modulating angiogenesis in tumor microenvironments and the wider implications that this may have in future therapies.

We look forward to your correspondence.

Prof. Tatiana V. Byzova
Dr. Michael G. McCoy
Guest Editor

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Published Papers (1 paper)

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15 pages, 3155 KiB  
Article
Homeoprotein Msx1-PIASy Interaction Inhibits Angiogenesis
by Myung Jin Son, Seung Bae Rho, Kwangbae Kim, Mijung Oh, Chaeyeon Son, Sang Yong Song and Kyoungsook Park
Cells 2020, 9(8), 1854; https://doi.org/10.3390/cells9081854 - 7 Aug 2020
Cited by 7 | Viewed by 2853
Abstract
Previously, we demonstrated that the homeoprotein Msx1 interaction with p53 inhibited tumor growth by inducing apoptosis. However, Msx1 can exert its tumor suppressive effect through the inhibition of angiogenesis since growth of the tumor relies on sufficient blood supply from the existing vessels [...] Read more.
Previously, we demonstrated that the homeoprotein Msx1 interaction with p53 inhibited tumor growth by inducing apoptosis. However, Msx1 can exert its tumor suppressive effect through the inhibition of angiogenesis since growth of the tumor relies on sufficient blood supply from the existing vessels to provide oxygen and nutrients for tumor growth. We hypothesized that the inhibition of tumor growth by Msx1 might be due to the inhibition of angiogenesis. Here, we explored the role of Msx1 in angiogenesis. Overexpression of Msx1 in HUVECs inhibited angiogenesis, and silencing of Msx1 by siRNA abrogated its anti-angiogenic effects. Furthermore, forced expression of Msx1 in mouse muscle tissue inhibited vessel sprouting, and application of an Ad-Msx1-transfected conditioned medium onto the chicken chorioallantoic membrane (CAM) led to a significant inhibition of new vessel formation. To explore the underlying mechanism of Msx1-mediated angiogenesis, yeast two-hybrid screening was performed, and we identified PIASy (protein inhibitor of activated STAT Y) as a novel Msx1-interacting protein. We mapped the homeodomain of Msx1 and the C-terminal domain of PIASy as respective interacting domains. Consistent with its anti-angiogenic function, overexpression of Msx1 suppressed the reporter activity of VEGF. Interestingly, PIASy stabilized Msx1 protein, whereas deletion of the Msx1-interacting domain in PIASy abrogated the inhibition of tube formation and the stabilization of Msx1 protein. Our findings suggest the functional importance of PIASy-Msx1 interaction in Msx1-mediated angiogenesis inhibition. Full article
(This article belongs to the Special Issue Angiogenesis in Cancer Therapy)
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