The Experts below are selected from a list of 35910 Experts worldwide ranked by ideXlab platform
Sophie Camilleribroet - One of the best experts on this subject based on the ideXlab platform.
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neutrophil extracellular trap associated ceacam1 as a putative therapeutic target to prevent metastatic progression of Colon Carcinoma
Journal of Immunology, 2020Co-Authors: Roni F Rayes, P Vourtzoumis, Bou Rjeily M, R Seth, F Bourdeau, Betty Giannias, Julie Berube, Y H Huang, Simon Rousseau, Sophie CamilleribroetAbstract:Neutrophils promote tumor growth and metastasis at multiple stages of cancer progression. One mechanism through which this occurs is via release of neutrophil extracellular traps (NETs). We have previously shown that NETs trap tumor cells in both the liver and the lung, increasing their adhesion and metastasis following postoperative complications. Multiple studies have since shown that NETs play a role in tumor progression and metastasis. NETs are composed of nuclear DNA-derived web-like structures decorated with neutrophil-derived proteins. However, it is unknown which, if any, of these NET-affiliated proteins is responsible for inducing the metastatic phenotype. In this study, we identify the NET-associated carcinoembryonic Ag cell adhesion molecule 1 (CEACAM1) as an essential element for this interaction. Indeed, blocking CEACAM1 on NETs, or knocking it out in a murine model, leads to a significant decrease in Colon Carcinoma cell adhesion, migration and metastasis. Thus, this work identifies NET-associated CEACAM1 as a putative therapeutic target to prevent the metastatic progression of Colon Carcinoma.
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neutrophil extracellular trap associated ceacam1 as a putative therapeutic target to prevent metastatic progression of Colon Carcinoma
Journal of Immunology, 2020Co-Authors: Roni F Rayes, P Vourtzoumis, Bou Rjeily M, R Seth, F Bourdeau, Betty Giannias, Julie Berube, Y H Huang, Simon Rousseau, Sophie CamilleribroetAbstract:Neutrophils promote tumor growth and metastasis at multiple stages of cancer progression. One mechanism through which this occurs is via release of neutrophil extracellular traps (NETs). We have previously shown that NETs trap tumor cells in both the liver and the lung, increasing their adhesion and metastasis following postoperative complications. Multiple studies have since shown that NETs play a role in tumor progression and metastasis. NETs are composed of nuclear DNA-derived web-like structures decorated with neutrophil-derived proteins. However, it is unknown which, if any, of these NET-affiliated proteins is responsible for inducing the metastatic phenotype. In this study, we identify the NET-associated carcinoembryonic Ag cell adhesion molecule 1 (CEACAM1) as an essential element for this interaction. Indeed, blocking CEACAM1 on NETs, or knocking it out in a murine model, leads to a significant decrease in Colon Carcinoma cell adhesion, migration and metastasis. Thus, this work identifies NET-associated CEACAM1 as a putative therapeutic target to prevent the metastatic progression of Colon Carcinoma.
Mohamed Jemaa - One of the best experts on this subject based on the ideXlab platform.
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inhibition of Colon Carcinoma cell migration following treatment with purified venom from lesser weever fish trachinus vipera
Cellular Physiology and Biochemistry, 2017Co-Authors: Myriann Fezai, Chaker Slaymi, Mossadok Benattia, Guido Kroemer, Florian Lang, Mohamed JemaaAbstract:Background: Injury by the sting of Lesser weever fish (Trachinus vipera) may lead to severe pain, edema or tissue necrosis. Cellular effects of the venom are still incompletely understood. Previous observations revealed that purified Lesser weever fish venom (LWFV) induces suicidal death of erythrocytes and HCT116 human Colon Carcinoma cells. The present study addressed the effect of the venom on Colon Carcinoma cell toxicity, shape and migration both in p53+/+ and/or p53-/- conditions. Methods: Cells were exposed to medium without or with 500 μg/ ml LWFV. Cell shape, cell area and circularity were visualized and quantified by fluorescence microscopy. Cell volume, granularity and cells toxicity were assessed via the apoptotic parameters dissipation of mitochondrial inner transmembrane potential, phosphatidylserine surface exposure and cell membrane permeabilization were measured utilizing flow cytometry. Cell migration was evaluated using wound healing assay and two-dimensional migration assay. Results: LWFV treatment was followed by a marked change of cell shape and size, significant decrease of cell area and circularity, significant impairment of cell migration, as well as induction of apoptosis after long exposition. Conclusions: LWFV exposure leads to cell shrinkage, increased granularity, apoptosis and impairment of cell migration, effects presumably contributing to LWFV-induced tissue injury. (Less)
Roni F Rayes - One of the best experts on this subject based on the ideXlab platform.
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neutrophil extracellular trap associated ceacam1 as a putative therapeutic target to prevent metastatic progression of Colon Carcinoma
Journal of Immunology, 2020Co-Authors: Roni F Rayes, P Vourtzoumis, Bou Rjeily M, R Seth, F Bourdeau, Betty Giannias, Julie Berube, Y H Huang, Simon Rousseau, Sophie CamilleribroetAbstract:Neutrophils promote tumor growth and metastasis at multiple stages of cancer progression. One mechanism through which this occurs is via release of neutrophil extracellular traps (NETs). We have previously shown that NETs trap tumor cells in both the liver and the lung, increasing their adhesion and metastasis following postoperative complications. Multiple studies have since shown that NETs play a role in tumor progression and metastasis. NETs are composed of nuclear DNA-derived web-like structures decorated with neutrophil-derived proteins. However, it is unknown which, if any, of these NET-affiliated proteins is responsible for inducing the metastatic phenotype. In this study, we identify the NET-associated carcinoembryonic Ag cell adhesion molecule 1 (CEACAM1) as an essential element for this interaction. Indeed, blocking CEACAM1 on NETs, or knocking it out in a murine model, leads to a significant decrease in Colon Carcinoma cell adhesion, migration and metastasis. Thus, this work identifies NET-associated CEACAM1 as a putative therapeutic target to prevent the metastatic progression of Colon Carcinoma.
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neutrophil extracellular trap associated ceacam1 as a putative therapeutic target to prevent metastatic progression of Colon Carcinoma
Journal of Immunology, 2020Co-Authors: Roni F Rayes, P Vourtzoumis, Bou Rjeily M, R Seth, F Bourdeau, Betty Giannias, Julie Berube, Y H Huang, Simon Rousseau, Sophie CamilleribroetAbstract:Neutrophils promote tumor growth and metastasis at multiple stages of cancer progression. One mechanism through which this occurs is via release of neutrophil extracellular traps (NETs). We have previously shown that NETs trap tumor cells in both the liver and the lung, increasing their adhesion and metastasis following postoperative complications. Multiple studies have since shown that NETs play a role in tumor progression and metastasis. NETs are composed of nuclear DNA-derived web-like structures decorated with neutrophil-derived proteins. However, it is unknown which, if any, of these NET-affiliated proteins is responsible for inducing the metastatic phenotype. In this study, we identify the NET-associated carcinoembryonic Ag cell adhesion molecule 1 (CEACAM1) as an essential element for this interaction. Indeed, blocking CEACAM1 on NETs, or knocking it out in a murine model, leads to a significant decrease in Colon Carcinoma cell adhesion, migration and metastasis. Thus, this work identifies NET-associated CEACAM1 as a putative therapeutic target to prevent the metastatic progression of Colon Carcinoma.
Myriann Fezai - One of the best experts on this subject based on the ideXlab platform.
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inhibition of Colon Carcinoma cell migration following treatment with purified venom from lesser weever fish trachinus vipera
Cellular Physiology and Biochemistry, 2017Co-Authors: Myriann Fezai, Chaker Slaymi, Mossadok Benattia, Guido Kroemer, Florian Lang, Mohamed JemaaAbstract:Background: Injury by the sting of Lesser weever fish (Trachinus vipera) may lead to severe pain, edema or tissue necrosis. Cellular effects of the venom are still incompletely understood. Previous observations revealed that purified Lesser weever fish venom (LWFV) induces suicidal death of erythrocytes and HCT116 human Colon Carcinoma cells. The present study addressed the effect of the venom on Colon Carcinoma cell toxicity, shape and migration both in p53+/+ and/or p53-/- conditions. Methods: Cells were exposed to medium without or with 500 μg/ ml LWFV. Cell shape, cell area and circularity were visualized and quantified by fluorescence microscopy. Cell volume, granularity and cells toxicity were assessed via the apoptotic parameters dissipation of mitochondrial inner transmembrane potential, phosphatidylserine surface exposure and cell membrane permeabilization were measured utilizing flow cytometry. Cell migration was evaluated using wound healing assay and two-dimensional migration assay. Results: LWFV treatment was followed by a marked change of cell shape and size, significant decrease of cell area and circularity, significant impairment of cell migration, as well as induction of apoptosis after long exposition. Conclusions: LWFV exposure leads to cell shrinkage, increased granularity, apoptosis and impairment of cell migration, effects presumably contributing to LWFV-induced tissue injury. (Less)
Ketao Jin - One of the best experts on this subject based on the ideXlab platform.
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antitumor effect of fp3 in combination with cetuximab on patient derived tumor tissue xenograft models of primary Colon Carcinoma and related lymphatic and hepatic metastases
International Journal of Molecular Medicine, 2012Co-Authors: Xiaofang Dong, Ketao Jin, Binbin Cui, Huanrong Lan, Na Han, Bojian Xie, Lisong Teng, Feilin CaoAbstract:FP3 is an engineered protein which contains the extracellular domain 2 of vascular endothelial growth factor (VEGF) receptor 1 (Flt-1) and the extracellular domain 3 and 4 of VEGF receptor 2 (Flk-1, KDR) fused to the Fc portion of human immunoglobulin G1. Previous studies have demonstrated its antiangiogenic effects in vitro and in vivo, and its antitumor activity in vivo. Cetuximab is a monoclonal antibody against epidermal growth factor (EGF) receptor. Combined inhibition of VEGF and EGF signaling may act additively or synergistically. In this study, patient-derived tumor tissue (PDTT) xenograft models of primary Colon Carcinoma and lymphatic and hepatic metastases were established for assessment of the antitumor activity of FP3 in combination with cetuximab. Xenografts were treated with FP3 and cetuximab, alone or in combination. After tumor growth was confirmed, volume and microvessel density in tumors were evaluated. Levels of VEGF, EGFR and PCNA in the tumor were examined by immunohistochemical staining, and levels of related cell signaling pathway proteins were examined by western blotting. FP3 in combination with cetuximab showed significant antitumor activity in three xenograft models (primary Colon Carcinoma, lymphatic metastasis and hepatic metastasis). The microvessel density in tumor tissues treated with FP3 in combination with cetuximab was lower compared to that of the control. Antitumor activity of FP3 in combination with cetuximab was significantly higher than that of each agent alone in two xenograft models (Colon Carcinoma lymphatic metastasis and hepatic metastasis). This study indicated that addition of FP3 to cetuximab significantly improved tumor growth inhibition in the PDTT xenograft models of Colon Carcinoma lymphatic and hepatic metastases. Combination anti-VEGF (FP3) and anti-EGFR (cetuximab) therapies may represent a novel therapeutic strategy for the management of metastatic Colon Carcinoma.
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assessment of a novel vegf targeted agent using patient derived tumor tissue xenograft models of Colon Carcinoma with lymphatic and hepatic metastases
PLOS ONE, 2011Co-Authors: Ketao Jin, Binbin Cui, Jing Zhang, Huanrong Lan, Na Han, Bojian Xie, Feilin Cao, Haohao Wang, Lisong TengAbstract:The lack of appropriate tumor models of primary tumors and corresponding metastases that can reliably predict for response to anticancer agents remains a major deficiency in the clinical practice of cancer therapy. It was the aim of our study to establish patient-derived tumor tissue (PDTT) xenograft models of Colon Carcinoma with lymphatic and hepatic metastases useful for testing of novel molecularly targeted agents. PDTT of primary Colon Carcinoma, lymphatic and hepatic metastases were used to create xenograft models. Hematoxylin and eosin staining, immunohistochemical staining, genome-wide gene expression analysis, pyrosequencing, qRT-PCR, and western blotting were used to determine the biological stability of the xenografts during serial transplantation compared with the original tumor tissues. Early passages of the PDTT xenograft models of primary Colon Carcinoma, lymphatic and hepatic metastases revealed a high degree of similarity with the original clinical tumor samples with regard to histology, immunohistochemistry, genes expression, and mutation status as well as mRNA expression. After we have ascertained that these xenografts models retained similar histopathological features and molecular signatures as the original tumors, drug sensitivities of the xenografts to a novel VEGF targeted agent, FP3 was evaluated. In this study, PDTT xenograft models of Colon Carcinoma with lymphatic and hepatic metastasis have been successfully established. They provide appropriate models for testing of novel molecularly targeted agents.
