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Biomedicines
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Tumor Microenvironment and Anti-angiogenic Therapies
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Tumor Microenvironment and Anti-angiogenic Therapies

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 7777

Special Issue Editors

Dr. Jerome Devy

E-Mail Website
Guest Editor
Matrice Extracellulaire et Dynamique Cellulaire, MEDyC, UMR 7369 CNRS-URCA, Université de Reims Champagne-Ardenne, 51687 Reims CEDEX 2, France
Interests: breast cancer; extracellular matrix; metastasis; cell adhesion; ECM receptors; proteolysis; angiogenesis; tumor microenvironment
Special Issues, Collections and Topics in MDPI journals
Dr. Benoit Langlois

E-Mail Website
Guest Editor
Matrice Extracellulaire et Dynamique Cellulaire, MEDyC, UMR 7369 CNRS-URCA, Université de Reims Champagne-Ardenne, 51687 Reims CEDEX 2, France
Interests: cancer cells; molecular biology; cancer research; cancer biology; proteins; signal transduction; cancer; apoptosis; signaling; cell signaling

Special Issue Information

Dear Colleagues,

Anti-angiogenic therapies should have revolutionized anti-tumoral strategies, but patient benefit is not the expected one. The aim of this Special Issue is to cover recent advances on the molecular and cellular mechanisms involved in tumor angiogenesis with a focus on major components of the tumor microenvironment, such as cancer associated fibroblasts, immune cells and endothelial cells progenitors and their close relation with the extracellular matrix. This special issue will also collect novel findings and reviews on the strategies aiming to control the stromal reaction of the tumor in the frame of anti-angiogenic and combinatorial treatments and the developments in the fields of tumor vessels and endothelial cell metabolism normalization that could open promising avenues to counter resistance mechanisms.

Dr. Jerome Devy
Dr. Benoit Langlois
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • tumor angiogenesis and vasculature
  • extracellular matrix and tumor microenvironment
  • angio-modulation through targeted therapies
  • adaptive response to treatments and resistance mechanisms

Published Papers (3 papers)

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Research

21 pages, 5844 KiB  
Article
AAV-Vectored Expression of the Vascular Normalizing Agents 3TSR and Fc3TSR, and the Anti-Angiogenic Bevacizumab Extends Survival in a Murine Model of End-Stage Epithelial Ovarian Carcinoma
by Ashley A. Stegelmeier, Lisa A. Santry, Matthew M. Guilleman, Kathy Matuszewska, Jessica A. Minott, Jacob G. E. Yates, Brenna A. Y. Stevens, Sylvia P. Thomas, Sierra Vanderkamp, Kiersten Hanada, Yanlong Pei, Amira D. Rghei, Jacob P. van Vloten, Madison Pereira, Brad Thompson, Pierre P. Major, James J. Petrik, Byram W. Bridle and Sarah K. Wootton
Biomedicines 2022, 10(2), 362; https://doi.org/10.3390/biomedicines10020362 - 02 Feb 2022
Cited by 3 | Viewed by 2621
Abstract
Epithelial ovarian cancer is the deadliest gynecological malignancy. The lack of effective treatments highlights the need for novel therapeutic interventions. The aim of this study was to investigate whether sustained adeno-associated virus (AAV) vector-mediated expression of vascular normalizing agents 3TSR and Fc3TSR and [...] Read more.
Epithelial ovarian cancer is the deadliest gynecological malignancy. The lack of effective treatments highlights the need for novel therapeutic interventions. The aim of this study was to investigate whether sustained adeno-associated virus (AAV) vector-mediated expression of vascular normalizing agents 3TSR and Fc3TSR and the antiangiogenic monoclonal antibody, Bevacizumab, with or without oncolytic virus treatment would improve survival in an orthotopic syngeneic mouse model of epithelial ovarian carcinoma. AAV vectors were administered 40 days post-tumor implantation and combined with oncolytic avian orthoavulavirus-1 (AOaV-1) 20 days later, at the peak of AAV-transgene expression, to ascertain whether survival could be extended. Flow cytometry conducted on blood samples, taken at an acute time point post-AOaV-1 administration (36 h), revealed a significant increase in activated NK cells in the blood of all mice that received AOaV-1. T cell analysis revealed a significant increase in CD8+ tumor specific T cells in the blood of AAV-Bevacizumab+AOaV-1 treated mice compared to control mice 10 days post AOaV-1 administration. Immunohistochemical staining of primary tumors harvested from a subset of mice euthanized 90 days post tumor implantation, when mice typically have large primary tumors, secondary peritoneal lesions, and extensive ascites fluid production, revealed that AAV-3TSR, AAV-Fc3TSR+AOaV-1, or AAV-Bevacizumab+AOaV-1 treated mice had significantly more tumor-infiltrating CD8+ T cells than PBS controls. Despite AAV-mediated transgene expression waning faster in tumor-bearing mice than in non-tumor bearing mice, all three of the AAV therapies significantly extended survival compared to control mice; with AAV-Bevacizumab performing the best in this model. However, combining AAV therapies with a single dose of AOaV-1 did not lead to significant extensions in survival compared to AAV therapies on their own, suggesting that additional doses of AOaV-1 may be required to improve efficacy in this model. These results suggest that vectorizing anti-angiogenic and vascular normalizing agents is a viable therapeutic option that warrants further investigation, including optimizing combination therapies. Full article
(This article belongs to the Special Issue Tumor Microenvironment and Anti-angiogenic Therapies)
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14 pages, 3587 KiB  
Article
WISP-3 Stimulates VEGF-C-Dependent Lymphangiogenesis in Human Chondrosarcoma Cells by Inhibiting miR-196a-3p Synthesis
by Chih-Yang Lin, Shih-Wei Wang, Jeng-Hung Guo, Huai-Ching Tai, Wen-Chun Sun, Cheng-Ta Lai, Chen-Yu Yang, Shih-Chia Liu, Yi-Chin Fong and Chih-Hsin Tang
Biomedicines 2021, 9(10), 1330; https://doi.org/10.3390/biomedicines9101330 - 27 Sep 2021
Cited by 4 | Viewed by 1939
Abstract
Chondrosarcoma is a malignant bone tumor with high metastatic potential. Lymphangiogenesis is a critical biological step in cancer metastasis. WNT1-inducible signaling pathway protein 3 (WISP-3) regulates angiogenesis and facilitates chondrosarcoma metastasis, but the role of WISP-3 in chondrosarcoma lymphangiogenesis is unclear. In this [...] Read more.
Chondrosarcoma is a malignant bone tumor with high metastatic potential. Lymphangiogenesis is a critical biological step in cancer metastasis. WNT1-inducible signaling pathway protein 3 (WISP-3) regulates angiogenesis and facilitates chondrosarcoma metastasis, but the role of WISP-3 in chondrosarcoma lymphangiogenesis is unclear. In this study, incubation of chondrosarcoma cells with WISP-3 increased the production of VEGF-C, an important lymphangiogenic factor. Conditioned medium from WISP-3-treated chondrosarcoma cells significantly enhanced lymphatic endothelial cell tube formation. WISP-3-induced stimulation of VEGF-C-dependent lymphangiogenesis inhibited miR-196a-3p synthesis in the ERK, JNK, and p38 signaling pathways. This evidence suggests that the WISP-3/VEGF-C axis is worth targeting in the treatment of lymphangiogenesis in human chondrosarcoma. Full article
(This article belongs to the Special Issue Tumor Microenvironment and Anti-angiogenic Therapies)
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17 pages, 3392 KiB  
Article
Concurrent Blockade of Endothelial EGFR and VEGF Signaling on Malignant Associated Pleural Fluid Induced Angiogenesis: From Clinic to Bench
by Wei-Teing Chen, Yu-Huei Lin, Chih-Ying Changchien, Ying Chen, Hsin-Han Chang, Wen-Chiuan Tsai, Hao-Chung Tsai, Chieh-Yung Wang, Ming-Sheng Shen, Li-Ting Cheng and Chen-Liang Tsai
Biomedicines 2021, 9(10), 1327; https://doi.org/10.3390/biomedicines9101327 - 26 Sep 2021
Cited by 2 | Viewed by 2507
Abstract
Malignant-associated pleural fluid (MAPF) represented an unsolved problem in advanced lung cancer. Our previous work characterized increased pleural angiogenesis in lung adenocarcinoma and the propensity of MAPF on endothelial angiogenesis. This study investigated the combined efficacy of the tyrosine kinase inhibitor (gefitinib) and [...] Read more.
Malignant-associated pleural fluid (MAPF) represented an unsolved problem in advanced lung cancer. Our previous work characterized increased pleural angiogenesis in lung adenocarcinoma and the propensity of MAPF on endothelial angiogenesis. This study investigated the combined efficacy of the tyrosine kinase inhibitor (gefitinib) and bevacizumab in opposing MAPF-induced angiogenesis. In lung adenocarcinoma patients with malignant pleural effusion (MPE), Kaplan–Meier analysis revealed the benefit of cotreatment with target therapy and bevacizumab. Increased EGFR expression was observed in the pleural microvessels of patients with lung adenocarcinoma both with and without mutations in EGFR. MAPF was obtained from lung adenocarcinoma patients both wild-type and mutant EGFRs. Total and phosphorylated EGFR were upregulated in HUVEC cultured with MAPF. Treatment with gefitinib as an EGFR inhibitor suppressed MAPF-induced endothelial migration and partially attenuated endothelial proliferation in both wild-type and mutant EGFR lung adenocarcinoma. Cotreatment with gefitinib and bevacizumab produced better inhibition of MAPF-induced endothelial angiogenesis than gefitinib alone in the mutant EGFR subgroup. Protein analysis of MAPF-derived exosomes revealed abundant EGFR and p-EGFR components that implied possible transfer to endothelial cells. Concluding Kaplan–Meier analysis and in vitro studies, the results indicated that the addition of bevacizumab on gefitinib treatment could suppress MAPF-induced angiogenesis in lung adenocarcinoma patients. Full article
(This article belongs to the Special Issue Tumor Microenvironment and Anti-angiogenic Therapies)
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