scholarly journals Chicken chorioallantoic membrane as a reliable model to evaluate osteosarcoma—an experimental approach using SaOS2 cell line

2015 ◽  
Vol 17 (1) ◽  
Author(s):  
Reji Manjunathan ◽  
Malathi Ragunathan
Keyword(s):  
Cell Line ◽  
Experimental Approach ◽  
Chorioallantoic Membrane ◽  
Saos2 Cell ◽  
Reliable Model ◽  
Chicken Chorioallantoic Membrane

Expression and Functional Analysis of Disintegrin from Agkistrodon Actus Venom.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3963-3963
Author(s):  
Xia Bai ◽  
Jianxin Fu ◽  
Jian Su ◽  
Lan Dai ◽  
Wei Zhang ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Recombinant Protein ◽  
Cell Line ◽  
Tumor Metastasis ◽  
Chorioallantoic Membrane ◽  
Cancer Cell Line ◽  
Dependent Manner ◽  
Inhibit Platelet Aggregation ◽  
Disintegrin Domain ◽  
Chicken Chorioallantoic Membrane

Abstract Disintegrin is a kind of small native peptides derived from the snake venom, containing RGD sequences. Its interaction with integrins, such as aIIbb3, anb3 and a5b1, can inhibit platelet aggregation. hinder the process of angiogenesis and tumor metastasis. In order to further investigate the function of disintegrin in platelet aggregation, cell adhesion and angiogenesis, the sequence encoding the disintegrin domain of agacutin was fused with enhanced green fluorencent protein(eGFP) and inserted in plasmid pQE-30. The recombinant protein was expressed in E.Coli M15 after induction by IPTG, amounting to 38% of the total bacterial protein. The cells expressing integrin such as breast cancer cell line MDA-MB-231 and endothelial cell line EA.hy926 can specifically bind to the recombinant GFP-disintegrin. Flow cytometry showed that the recombinant protein could bind to platelet specfically and could compete with anti-b3 integrin monoclonal antibody CD61. Moreover, the recombinant protein could inhibit platelet aggregation induced by collagen and ADP in a dose-dependent manner, but had no ability to impede the platelet aggregation induced by Ristocetin. Meanwhile, it could inhibit cell (MDA-MB-231 and EA.hy926) adhesion to fibronectin with inhibition rate of 69% and 48%, respectively. Finally, it could induce apoptosis of EA.hy926 endothelial cells and inhibit the angiogenesis on chicken chorioallantoic membrane mode. As a result, it is demonstrated that GFP-disintegrin has the combined quality of its disparate components and can serve as a novel tool for study of tumor and angiogenesis. In addition, the recombinant protein can efficiently inhibit platelet aggregation and angiogenesis, which will be useful for designing the potential drug for anti-thrombosis and anti-tumor metastasis.

scholarly journals The Chicken Chorioallantoic Membrane Tumor Assay as a Relevant In Vivo Model to Study the Impact of Hypoxia on Tumor Progression and Metastasis

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1093
Author(s):  
Kelly Harper ◽  
Anna Yatsyna ◽  
Martine Charbonneau ◽  
Karine Brochu-Gaudreau ◽  
Alexis Perreault ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Progression ◽  
Cell Line ◽  
Tumor Therapy ◽  
Chorioallantoic Membrane ◽  
Human Tumor ◽  
Chicken Chorioallantoic Membrane ◽  
The Impact ◽  
Cam Model

Hypoxia in the tumor microenvironment is a negative prognostic factor associated with tumor progression and metastasis, and therefore represents an attractive therapeutic target for anti-tumor therapy. To test the effectiveness of novel hypoxia-targeting drugs, appropriate preclinical models that recreate tumor hypoxia are essential. The chicken ChorioAllantoic Membrane (CAM) assay is increasingly used as a rapid cost-effective in vivo drug-testing platform that recapitulates many aspects of human cancers. However, it remains to be determined whether this model recreates the hypoxic microenvironment of solid tumors. To detect hypoxia in the CAM model, the hypoxic marker pimonidazole was injected into the vasculature of tumor-bearing CAM, and hypoxia-dependent gene expression was analyzed. We observed that the CAM model effectively supports the development of hypoxic zones in a variety of human tumor cell line-derived and patient’s tumor fragment-derived xenografts. The treatment of both patient and cell line-derived CAM xenografts with modulators of angiogenesis significantly altered the formation of hypoxic zones within the xenografts. Furthermore, the changes in hypoxia translated into modulated levels of chick liver metastasis as measured by Alu-based assay. These findings demonstrate that the CAM xenograft model is a valuable in vivo platform for studying hypoxia that could facilitate the identification and testing of drugs targeting this tumor microenvironment.

Inhibition by doxycycline of angiogenesis in the chicken chorioallantoic membrane (CAM)

2005 ◽  
Vol 56 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Mary Richardson ◽  
David Wong ◽  
Samantha Lacroix ◽  
Jolanta Stanisz ◽  
Gurmit Singh
Keyword(s):  
Chorioallantoic Membrane ◽  
Chicken Chorioallantoic Membrane

scholarly journals Angiotropism of Human Melanoma: Studies Involving In Transit and Other Cutaneous Metastases and the Chicken Chorioallantoic Membrane

2006 ◽  
Vol 28 (3) ◽  
pp. 187-193 ◽  
Author(s):  
Claire Lugassy ◽  
Stephen E. Vernon ◽  
Klaus Busam ◽  
Jean A. Engbring ◽  
Danny R. Welch ◽  
...  
Keyword(s):  
Chorioallantoic Membrane ◽  
Human Melanoma ◽  
Cutaneous Metastases ◽  
In Transit ◽  
Chicken Chorioallantoic Membrane

scholarly journals An antagonist of integrin alpha v beta 3 prevents maturation of blood vessels during embryonic neovascularization

1995 ◽  
Vol 108 (7) ◽  
pp. 2655-2661 ◽  
Author(s):  
C.J. Drake ◽  
D.A. Cheresh ◽  
C.D. Little
Keyword(s):  
Experimental Data ◽  
Monoclonal Antibody ◽  
Blood Vessels ◽  
Chorioallantoic Membrane ◽  
Normal Pattern ◽  
Basal Surface ◽  
Lumen Formation ◽  
Vessel Development ◽  
Alpha V Beta 3 ◽  
Chicken Chorioallantoic Membrane

Experimental data in this study demonstrate that integrin alpha v beta 3 is fundamentally involved in the maturation of blood vessels during embryonic neovascularization (vasculogenesis). Integrin alpha v beta 3 was specifically expressed on the surface of angioblasts during vessel development in quail embryos and vitronectin, a ligand for alpha v beta 3, localized to the basal surface of these cells. More importantly, microinjection of the anti-alpha v beta 3 monoclonal antibody, LM609, disrupted the normal pattern of vascular development. After exposure to LM609 the angioblasts in experimental embryos appeared as clusters of rounded cells lacking normal cellular protrusions. This led to disruption of lumen formation and abnormal vessel patterning. These findings demonstrate that during vasculogenesis ligation of integrin alpha v beta 3 on the surface of primordial endothelial cells is critical for the differentiation and maturation of blood vessels. Similar studies on chicken chorioallantoic membrane showed that LM609 blocks angiogenesis. Together the two studies suggest that integrin alpha v beta 3 plays a role in neovascularization of tissues.

scholarly journals STAT3/5 Inhibitors Suppress Proliferation in Bladder Cancer and Enhance Oncolytic Adenovirus Therapy

2020 ◽  
Vol 21 (3) ◽  
pp. 1106 ◽  
Author(s):  
Sruthi V. Hindupur ◽  
Sebastian C. Schmid ◽  
Jana Annika Koch ◽  
Ahmed Youssef ◽  
Eva-Maria Baur ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Cycle Progression ◽  
Chorioallantoic Membrane ◽  
Oncolytic Adenovirus ◽  
Cycle Progression ◽  
Cellular Processes ◽  
Division Cell ◽  
Chicken Chorioallantoic Membrane ◽  
Cam Model ◽  
Phosphorylated Stat3

The JAK-STAT signalling pathway regulates cellular processes like cell division, cell death and immune regulation. Dysregulation has been identified in solid tumours and STAT3 activation is a marker for poor outcome. The aim of this study was to explore potential therapeutic strategies by targeting this pathway in bladder cancer (BC). High STAT3 expression was detected in 51.3% from 149 patient specimens with invasive bladder cancer by immunohistochemistry. Protein expression of JAK, STAT and downstream targets were confirmed in 10 cell lines. Effects of the JAK inhibitors Ruxolitinib and BSK-805, and STAT3/5 inhibitors Stattic, Nifuroxazide and SH-4-54 were analysed by cell viability assays, immunoblotting, apoptosis and cell cycle progression. Treatment with STAT3/5 but not JAK1/2 inhibitors reduced survival, levels of phosphorylated STAT3 and Cyclin-D1 and increased apoptosis. Tumour xenografts, using the chicken chorioallantoic membrane (CAM) model responded to Stattic monotherapy. Combination of Stattic with Cisplatin, Docetaxel, Gemcitabine, Paclitaxel and CDK4/6 inhibitors showed additive effects. The combination of Stattic with the oncolytic adenovirus XVir-N-31 increased viral replication and cell lysis. Our results provide evidence that inhibitors against STAT3/5 are promising as novel mono- and combination therapy in bladder cancer.

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