scholarly journals Role of Angiopoietins in Development of Cancer and Neoplasia Associated with Viral Infection

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 457 ◽  
Author(s):  
Xiaolan Yu ◽  
Fengchun Ye
Keyword(s):  
Viral Infection ◽  
Tumor Angiogenesis ◽  
Vascular Endothelial ◽  
Oncogenic Viruses ◽  
Promote Tumor Cell ◽  
Promote Tumor Cell Invasion ◽  
Vessel Maturation ◽  
Tyrosine Protein Kinase ◽  
Angiopoietin 2 ◽  
Endothelial Growth Factor

Angiopoietin/tyrosine protein kinase receptor Tie-2 signaling in endothelial cells plays an essential role in angiogenesis and wound healing. Angiopoietin-1 (Ang-1) is crucial for blood vessel maturation while angiopoietin-2 (Ang-2), in collaboration with vascular endothelial growth factor (VEGF), initiates angiogenesis by destabilizing existing blood vessels. In healthy people, the Ang-1 level is sustained while Ang-2 expression is restricted. In cancer patients, Ang-2 level is elevated, which correlates with poor prognosis. Ang-2 not only drives tumor angiogenesis but also attracts infiltration of myeloid cells. The latter rapidly differentiate into tumor stromal cells that foster tumor angiogenesis and progression, and weaken the host’s anti-tumor immunity. Moreover, through integrin signaling, Ang-2 induces expression of matrix metallopeptidases (MMPs) to promote tumor cell invasion and metastasis. Many oncogenic viruses induce expression of Ang-2 to promote development of neoplasia associated with viral infection. Multiple Ang-2 inhibitors exhibit remarkable anti-tumor activities, further highlighting the importance of Ang-2 in cancer development.

The Role of Vascular Endothelial Growth Factor in Tumor Angiogenesis

1998 ◽  
pp. 305-318
Author(s):  
Georg Breier ◽  
Annette Damert ◽  
Sabine Blum ◽  
Ernst Reichmann ◽  
Karl H. Plate ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tumor Angiogenesis ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Placental Growth Factor-1 Attenuates Vascular Endothelial Growth Factor-A–Dependent Tumor Angiogenesis during β Cell Carcinogenesis

2007 ◽  
Vol 67 (22) ◽  
pp. 10840-10848 ◽  
Author(s):  
Tibor Schomber ◽  
Lucie Kopfstein ◽  
Valentin Djonov ◽  
Imke Albrecht ◽  
Vanessa Baeriswyl ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tumor Angiogenesis ◽  
Placental Growth Factor ◽  
Vascular Endothelial ◽  
Β Cell ◽  
Endothelial Growth Factor

scholarly journals Harmine suppresses bladder tumor growth by suppressing vascular endothelial growth factor receptor 2-mediated angiogenesis

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Cai Hai-rong ◽  
Huang Xiang ◽  
Zhang Xiao-rong
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Bladder Cancer ◽  
Growth Factor ◽  
Natural Product ◽  
Tumor Angiogenesis ◽  
Bladder Tumor ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Human Bladder ◽  
Endothelial Growth Factor

Abstract Angiogenesis is a vital step during the process of oncogenesis of a lot of tumors, with no exception in bladder cancer. One of the useful strategies for the development of new drugs against cancer is targeting angiogenesis. In the present study, we found that a small-molecule natural product, which belonged to the β-carboline alkaloid, named harmine, could strongly inhibit tumor angiogenesis thus exhibiting its ideal treatment efficacy in bladder cancer. In vivo study verified that harmine had the effect of inhibition on human bladder tumor xenograft growth. The inhibitory effect of harmine to bladder cancer growth was coordinated by the effects shown on angiogenesis. To further explore the pharmacological activities of harmine, we tested harmine’s influence on blood vessel formation and found that harmine effectively blocked the microvessel sprouting in rat aortic ring assay when stimulated by vascular endothelial growth factor (VEGF). Furthermore, harmine inhibited human umbilical vein endothelial cell (HUVEC) proliferation as well as chemotactic motility, and when we treated HUVEC cell with harmine, the formation of capillary-like structures was also restrained. Moreover, harmine induced bladder cancer cell apoptosis through triggering the caspase-dependent apoptotic pathway and the downstream vascular endothelial growth factor receptor 2 (VEGFR2) kinase pathway was down-regulated, thus suppressing tumor development signals. Herein, our study demonstrated that natural product harmine might have potential in curing human bladder tumor because of its pharmacological function on tumor angiogenesis, trigged by VEGFR2 signaling pathways.

scholarly journals Effect of Weight Loss Surgery on Biomarkers of Angiogenesis in Obese Patients

2020 ◽  
Vol 30 (9) ◽  
pp. 3417-3425 ◽  
Author(s):  
Maciej Wiewiora ◽  
Anna Mertas ◽  
Marek Gluck ◽  
Alicja Nowowiejska-Wiewiora ◽  
Zenon Czuba ◽  
...  
Keyword(s):  
Weight Loss ◽  
Growth Factor ◽  
Weight Loss Surgery ◽  
Significant Negative Correlation ◽  
Vascular Endothelial ◽  
Obese Patients ◽  
Platelet Endothelial Cell Adhesion ◽  
Angiopoietin 2 ◽  
Endothelial Growth Factor ◽  
Circulating Levels

Abstract Background The present study aims to clarify the effects of weight loss on biomarkers associated with angiogenesis in patients who underwent laparoscopic sleeve gastrectomy (SG) or adjustable gastric banding (LAGB) in the 12-month follow-up study. Materials and Methods We studied 24 obese patients who underwent laparoscopic weight loss surgery, 13 of whom underwent SG and 11 of whom underwent LAGB. We evaluated the circulating level of angiogenesis biomarkers preoperatively and 12 months after surgery. Results Before surgery, the following angiogenic circulating factors were significantly higher than those of healthy subjects: angiopoietin 2 (ANG-2) (p < .05), granulocyte colony-stimulating factor (G-CSF) (p < .05), hepatocyte growth factor (HGF) (p < .01), platelet endothelial cell adhesion molecule (PECAM-1) (p < .01), and vascular endothelial growth factor (VEGF) (p < .05). The following angiogenesis biomarkers decreased significantly after weight loss compared with their baseline values: ANG-2 (p < .05), follistatin (p < .05), HGF (p < .01), PECAM-1 (p < .01), and VEGF (p < .05). There were no significant differences in the circulating levels of angiogenesis biomarkers between individuals who underwent SG and those who underwent LAGB; however, HGF, PECAM-1, and VEGF tended to be lower after SG. %BMI correlated negatively with HGF, PECAM-1, and VEGF. A similar significant negative correlation was found for %WL and %EWL. WHR correlated with PDGF-B and VEGF. Conclusions We concluded that weight loss surgery induces the changes of circulating levels of angiogenesis biomarkers in obese patients. The changes in angiogenesis status in obese patients who lost weight after bariatric surgery depended on the amount of weight loss.

scholarly journals Future treatments for hereditary hemorrhagic telangiectasia

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Florian Robert ◽  
Agnès Desroches-Castan ◽  
Sabine Bailly ◽  
Sophie Dupuis-Girod ◽  
Jean-Jacques Feige
Keyword(s):  
Hereditary Hemorrhagic Telangiectasia ◽  
Vascular Endothelial ◽  
Protein Receptor ◽  
Morphogenetic Protein ◽  
Receptor Like Kinase ◽  
Recent Developments ◽  
Frequent Mutations ◽  
Transcriptional Complex ◽  
Angiopoietin 2 ◽  
Endothelial Growth Factor

AbstractHereditary Hemorrhagic Telangiectasia (HHT), also known as Rendu-Osler syndrome, is a genetic vascular disorder affecting 1 in 5000–8000 individuals worldwide. This rare disease is characterized by various vascular defects including epistaxis, blood vessel dilations (telangiectasia) and arteriovenous malformations (AVM) in several organs. About 90% of the cases are associated with heterozygous mutations of ACVRL1 or ENG genes, that respectively encode a bone morphogenetic protein receptor (activin receptor-like kinase 1, ALK1) and a co-receptor named endoglin. Less frequent mutations found in the remaining 10% of patients also affect the gene SMAD4 which is part of the transcriptional complex directly activated by this pathway. Presently, the therapeutic treatments for HHT are intended to reduce the symptoms of the disease. However, recent progress has been made using drugs that target VEGF (vascular endothelial growth factor) and the angiogenic pathway with the use of bevacizumab (anti-VEGF antibody). Furthermore, several exciting high-throughput screenings and preclinical studies have identified new molecular targets directly related to the signaling pathways affected in the disease. These include FKBP12, PI3-kinase and angiopoietin-2. This review aims at reporting these recent developments that should soon allow a better care of HHT patients.

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