The Experts below are selected from a list of 309 Experts worldwide ranked by ideXlab platform
Zhihua Liu - One of the best experts on this subject based on the ideXlab platform.
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Overexpression of stefin A in human esophageal squamous cell carcinoma cells inhiBits tumor cell growth, angiogenesis, invasion, and metastasis.
Clinical cancer research : an official journal of the American Association for Cancer Research, 2005Co-Authors: Fang Ding, Liyong Zhang, Zhongmin Liu, Aiping Luo, Mingrong Wang, Qimin Zhan, Zhihua LiuAbstract:Evidence is accumulating that an inverse correlation exists Between stefin A level and malignant progression. The aim of this study is to investigate the role of stefin A in human esophageal squamous cell carcinoma cells and to evaluate the possiBility of stefin A for cancer therapy. We staBly transfected stefin A cDNA into human EC9706 or KYSE150 esophageal squamous cell carcinoma cells. SuBsequently, we evaluated the effect of stefin A overexpression on cell growth, <B>CathepsinB> B activity, cell motility and invasion, tumor growth, and metastasis. Immunoanalysis was done to assess the expression of factor VIII and to support the localization of stefin A and <B>CathepsinB> B. We also evaluated the effect of CA074Me, a selective memBrane-permeant <B>CathepsinB> B inhiBitor. Both transfection of stefin A and treatment with 10 micromol/L CA074Me significantly reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. ComBination of Both further reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. Overexpression of stefin A delayed the in vitro and in vivo growth of cells and significantly inhiBited lung metastasis compared with 50% of lung metastasis in xenograft mice from EC9706 or empty vector cells. Transfection with stefin A showed a dramatic reduction of factor VIII staining in the tumors of xenograft mice. Our data strongly indicate that stefin A plays an important role in the growth, angiogenesis, invasion, and metastasis of human esophageal squamous cell carcinoma cells and suggest that stefin A may Be useful in cancer therapy.
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Overexpression of stefin A in human esophageal squamous cell carcinoma cells inhiBits tumor cell growth, angiogenesis, invasion, and metastasis.
Clinical Cancer Research, 2005Co-Authors: Fang Ding, Liyong Zhang, Zhongmin Liu, Aiping Luo, Mingrong Wang, Qimin Zhan, Zhihua LiuAbstract:Purpose: Evidence is accumulating that an inverse correlation exists Between stefin A level and malignant progression. The aim of this study is to investigate the role of stefin A in human esophageal squamous cell carcinoma cells and to evaluate the possiBility of stefin A for cancer therapy. Experimental Design: We staBly transfected stefin A cDNA into human EC9706 or KYSE150 esophageal squamous cell carcinoma cells. SuBsequently, we evaluated the effect of stefin A overexpression on cell growth, <B>CathepsinB> B activity, cell motility and invasion, tumor growth, and metastasis. Immunoanalysis was done to assess the expression of factor VIII and to support the localization of stefin A and <B>CathepsinB> B. We also evaluated the effect of CA074Me, a selective memBrane-permeant <B>CathepsinB> B inhiBitor. Results: Both transfection of stefin A and treatment with 10 μmol/L CA074Me significantly reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. ComBination of Both further reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. Overexpression of stefin A delayed the in vitro and in vivo growth of cells and significantly inhiBited lung metastasis compared with 50% of lung metastasis in xenograft mice from EC9706 or empty vector cells. Transfection with stefin A showed a dramatic reduction of factor VIII staining in the tumors of xenograft mice. Conclusions: Our data strongly indicate that stefin A plays an important role in the growth, angiogenesis, invasion, and metastasis of human esophageal squamous cell carcinoma cells and suggest that stefin A may Be useful in cancer therapy.
Fang Ding - One of the best experts on this subject based on the ideXlab platform.
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Overexpression of stefin A in human esophageal squamous cell carcinoma cells inhiBits tumor cell growth, angiogenesis, invasion, and metastasis.
Clinical cancer research : an official journal of the American Association for Cancer Research, 2005Co-Authors: Fang Ding, Liyong Zhang, Zhongmin Liu, Aiping Luo, Mingrong Wang, Qimin Zhan, Zhihua LiuAbstract:Evidence is accumulating that an inverse correlation exists Between stefin A level and malignant progression. The aim of this study is to investigate the role of stefin A in human esophageal squamous cell carcinoma cells and to evaluate the possiBility of stefin A for cancer therapy. We staBly transfected stefin A cDNA into human EC9706 or KYSE150 esophageal squamous cell carcinoma cells. SuBsequently, we evaluated the effect of stefin A overexpression on cell growth, <B>CathepsinB> B activity, cell motility and invasion, tumor growth, and metastasis. Immunoanalysis was done to assess the expression of factor VIII and to support the localization of stefin A and <B>CathepsinB> B. We also evaluated the effect of CA074Me, a selective memBrane-permeant <B>CathepsinB> B inhiBitor. Both transfection of stefin A and treatment with 10 micromol/L CA074Me significantly reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. ComBination of Both further reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. Overexpression of stefin A delayed the in vitro and in vivo growth of cells and significantly inhiBited lung metastasis compared with 50% of lung metastasis in xenograft mice from EC9706 or empty vector cells. Transfection with stefin A showed a dramatic reduction of factor VIII staining in the tumors of xenograft mice. Our data strongly indicate that stefin A plays an important role in the growth, angiogenesis, invasion, and metastasis of human esophageal squamous cell carcinoma cells and suggest that stefin A may Be useful in cancer therapy.
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Overexpression of stefin A in human esophageal squamous cell carcinoma cells inhiBits tumor cell growth, angiogenesis, invasion, and metastasis.
Clinical Cancer Research, 2005Co-Authors: Fang Ding, Liyong Zhang, Zhongmin Liu, Aiping Luo, Mingrong Wang, Qimin Zhan, Zhihua LiuAbstract:Purpose: Evidence is accumulating that an inverse correlation exists Between stefin A level and malignant progression. The aim of this study is to investigate the role of stefin A in human esophageal squamous cell carcinoma cells and to evaluate the possiBility of stefin A for cancer therapy. Experimental Design: We staBly transfected stefin A cDNA into human EC9706 or KYSE150 esophageal squamous cell carcinoma cells. SuBsequently, we evaluated the effect of stefin A overexpression on cell growth, <B>CathepsinB> B activity, cell motility and invasion, tumor growth, and metastasis. Immunoanalysis was done to assess the expression of factor VIII and to support the localization of stefin A and <B>CathepsinB> B. We also evaluated the effect of CA074Me, a selective memBrane-permeant <B>CathepsinB> B inhiBitor. Results: Both transfection of stefin A and treatment with 10 μmol/L CA074Me significantly reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. ComBination of Both further reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. Overexpression of stefin A delayed the in vitro and in vivo growth of cells and significantly inhiBited lung metastasis compared with 50% of lung metastasis in xenograft mice from EC9706 or empty vector cells. Transfection with stefin A showed a dramatic reduction of factor VIII staining in the tumors of xenograft mice. Conclusions: Our data strongly indicate that stefin A plays an important role in the growth, angiogenesis, invasion, and metastasis of human esophageal squamous cell carcinoma cells and suggest that stefin A may Be useful in cancer therapy.
Farshid Hassanzadeh - One of the best experts on this subject based on the ideXlab platform.
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Targeted Nanoparticles for Co-delivery of 5-FU and Nitroxoline, a <B>CathepsinB> B InhiBitor, in HepG2 Cells of Hepatocellular Carcinoma.
Anti-cancer agents in medicinal chemistry, 2020Co-Authors: Jaleh Varshosaz, Monireh M. Fard, Mina Mirian, Farshid HassanzadehAbstract:The first choice of treatment in Hepatocellular Carcinoma (HCC) is 5-fluorouracil (5-FU). Nitroxoline (NIT), a potent inhiBitor of <B>CathepsinB> B, impairs tumor progression By decreased extracellular matrix degradation. The oBjective of the current project was designed to target nanoparticles for co-delivery of 5-FU and NIT in order to enhance the 5-FU cytotoxic effects and reduce the metastatic properties of HepG2 cells. 5-FU and NIT were loaded in chitosan-chondroitin nanoparticles. To target the CD44 receptors of HepG2 cells, Hyaluronic Acid (HA) was conjugated to the chondroitin By adipic acid dihydrazide and the conjugation was confirmed By FTIR and 1HNMR. After physicochemical characterization and optimization of the processing variaBles, MTT assay was done on HepG2 and NIH3T3 cell lines to determine the cytotoxic properties of HA targeted nanoparticles. Migration of the cells was studied to compare the co-delivery of the drugs with each drug alone. The optimized nanoparticles showed the particle size of 244.7±16.3nm, PDI of 0.30±0.03, drug entrapment efficiency of 46.3±5.0% for 5-FU and 75.1±0.9% for NIT. The drug release efficiency up to 8 hours was aBout 37.6±0.9% for 5-FU and 62.9±0.7% for NIT. The co-delivery of 5-FU and NIT in targeted nanoparticles showed significantly more cytotoxicity than the mixture of the two free drugs, non-targeted nanoparticles or each drug alone and reduced the IC50 value of 5-FU from 3.31±0.65μg/ml to 0.17±0.03μg/ml and the migration of HepG2 cells was also reduced to five-fold. Co-delivery of 5-FU and NIT By HA targeted chitosan-chondroitin nanoparticles may Be promising in HCC. Copyright© Bentham Science PuBlishers; For any queries, please email at epuB@Benthamscience.net.
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targeted nanoparticles for co delivery of 5 fu and nitroxoline a <B>CathepsinB> B inhiBitor in hepg2 cells of hepatocellular carcinoma
Anti-cancer Agents in Medicinal Chemistry, 2020Co-Authors: Jaleh Varshosaz, Monireh M. Fard, Mina Mirian, Farshid HassanzadehAbstract:BACKGROUND The first choice of treatment in Hepatocellular Carcinoma (HCC) is 5-fluorouracil (5-FU). Nitroxoline (NIT), a potent inhiBitor of <B>CathepsinB> B, impairs tumor progression By decreased extracellular matrix degradation. The oBjective of the current project was designed to target nanoparticles for co-delivery of 5-FU and NIT in order to enhance the 5-FU cytotoxic effects and reduce the metastatic properties of HepG2 cells. METHODS 5-FU and NIT were loaded in chitosan-chondroitin nanoparticles. To target the CD44 receptors of HepG2 cells, Hyaluronic Acid (HA) was conjugated to the chondroitin By adipic acid dihydrazide and the conjugation was confirmed By FTIR and 1HNMR. After physicochemical characterization and optimization of the processing variaBles, MTT assay was done on HepG2 and NIH3T3 cell lines to determine the cytotoxic properties of HA targeted nanoparticles. Migration of the cells was studied to compare the co-delivery of the drugs with each drug alone. RESULTS The optimized nanoparticles showed the particle size of 244.7±16.3nm, PDI of 0.30±0.03, drug entrapment efficiency of 46.3±5.0% for 5-FU and 75.1±0.9% for NIT. The drug release efficiency up to 8 hours was aBout 37.6±0.9% for 5-FU and 62.9±0.7% for NIT. The co-delivery of 5-FU and NIT in targeted nanoparticles showed significantly more cytotoxicity than the mixture of the two free drugs, non-targeted nanoparticles or each drug alone and reduced the IC50 value of 5-FU from 3.31±0.65μg/ml to 0.17±0.03μg/ml and the migration of HepG2 cells was also reduced to five-fold. CONCLUSION Co-delivery of 5-FU and NIT By HA targeted chitosan-chondroitin nanoparticles may Be promising in HCC.
Mingrong Wang - One of the best experts on this subject based on the ideXlab platform.
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Overexpression of stefin A in human esophageal squamous cell carcinoma cells inhiBits tumor cell growth, angiogenesis, invasion, and metastasis.
Clinical cancer research : an official journal of the American Association for Cancer Research, 2005Co-Authors: Fang Ding, Liyong Zhang, Zhongmin Liu, Aiping Luo, Mingrong Wang, Qimin Zhan, Zhihua LiuAbstract:Evidence is accumulating that an inverse correlation exists Between stefin A level and malignant progression. The aim of this study is to investigate the role of stefin A in human esophageal squamous cell carcinoma cells and to evaluate the possiBility of stefin A for cancer therapy. We staBly transfected stefin A cDNA into human EC9706 or KYSE150 esophageal squamous cell carcinoma cells. SuBsequently, we evaluated the effect of stefin A overexpression on cell growth, <B>CathepsinB> B activity, cell motility and invasion, tumor growth, and metastasis. Immunoanalysis was done to assess the expression of factor VIII and to support the localization of stefin A and <B>CathepsinB> B. We also evaluated the effect of CA074Me, a selective memBrane-permeant <B>CathepsinB> B inhiBitor. Both transfection of stefin A and treatment with 10 micromol/L CA074Me significantly reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. ComBination of Both further reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. Overexpression of stefin A delayed the in vitro and in vivo growth of cells and significantly inhiBited lung metastasis compared with 50% of lung metastasis in xenograft mice from EC9706 or empty vector cells. Transfection with stefin A showed a dramatic reduction of factor VIII staining in the tumors of xenograft mice. Our data strongly indicate that stefin A plays an important role in the growth, angiogenesis, invasion, and metastasis of human esophageal squamous cell carcinoma cells and suggest that stefin A may Be useful in cancer therapy.
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Overexpression of stefin A in human esophageal squamous cell carcinoma cells inhiBits tumor cell growth, angiogenesis, invasion, and metastasis.
Clinical Cancer Research, 2005Co-Authors: Fang Ding, Liyong Zhang, Zhongmin Liu, Aiping Luo, Mingrong Wang, Qimin Zhan, Zhihua LiuAbstract:Purpose: Evidence is accumulating that an inverse correlation exists Between stefin A level and malignant progression. The aim of this study is to investigate the role of stefin A in human esophageal squamous cell carcinoma cells and to evaluate the possiBility of stefin A for cancer therapy. Experimental Design: We staBly transfected stefin A cDNA into human EC9706 or KYSE150 esophageal squamous cell carcinoma cells. SuBsequently, we evaluated the effect of stefin A overexpression on cell growth, <B>CathepsinB> B activity, cell motility and invasion, tumor growth, and metastasis. Immunoanalysis was done to assess the expression of factor VIII and to support the localization of stefin A and <B>CathepsinB> B. We also evaluated the effect of CA074Me, a selective memBrane-permeant <B>CathepsinB> B inhiBitor. Results: Both transfection of stefin A and treatment with 10 μmol/L CA074Me significantly reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. ComBination of Both further reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. Overexpression of stefin A delayed the in vitro and in vivo growth of cells and significantly inhiBited lung metastasis compared with 50% of lung metastasis in xenograft mice from EC9706 or empty vector cells. Transfection with stefin A showed a dramatic reduction of factor VIII staining in the tumors of xenograft mice. Conclusions: Our data strongly indicate that stefin A plays an important role in the growth, angiogenesis, invasion, and metastasis of human esophageal squamous cell carcinoma cells and suggest that stefin A may Be useful in cancer therapy.
Liyong Zhang - One of the best experts on this subject based on the ideXlab platform.
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Overexpression of stefin A in human esophageal squamous cell carcinoma cells inhiBits tumor cell growth, angiogenesis, invasion, and metastasis.
Clinical cancer research : an official journal of the American Association for Cancer Research, 2005Co-Authors: Fang Ding, Liyong Zhang, Zhongmin Liu, Aiping Luo, Mingrong Wang, Qimin Zhan, Zhihua LiuAbstract:Evidence is accumulating that an inverse correlation exists Between stefin A level and malignant progression. The aim of this study is to investigate the role of stefin A in human esophageal squamous cell carcinoma cells and to evaluate the possiBility of stefin A for cancer therapy. We staBly transfected stefin A cDNA into human EC9706 or KYSE150 esophageal squamous cell carcinoma cells. SuBsequently, we evaluated the effect of stefin A overexpression on cell growth, <B>CathepsinB> B activity, cell motility and invasion, tumor growth, and metastasis. Immunoanalysis was done to assess the expression of factor VIII and to support the localization of stefin A and <B>CathepsinB> B. We also evaluated the effect of CA074Me, a selective memBrane-permeant <B>CathepsinB> B inhiBitor. Both transfection of stefin A and treatment with 10 micromol/L CA074Me significantly reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. ComBination of Both further reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. Overexpression of stefin A delayed the in vitro and in vivo growth of cells and significantly inhiBited lung metastasis compared with 50% of lung metastasis in xenograft mice from EC9706 or empty vector cells. Transfection with stefin A showed a dramatic reduction of factor VIII staining in the tumors of xenograft mice. Our data strongly indicate that stefin A plays an important role in the growth, angiogenesis, invasion, and metastasis of human esophageal squamous cell carcinoma cells and suggest that stefin A may Be useful in cancer therapy.
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Overexpression of stefin A in human esophageal squamous cell carcinoma cells inhiBits tumor cell growth, angiogenesis, invasion, and metastasis.
Clinical Cancer Research, 2005Co-Authors: Fang Ding, Liyong Zhang, Zhongmin Liu, Aiping Luo, Mingrong Wang, Qimin Zhan, Zhihua LiuAbstract:Purpose: Evidence is accumulating that an inverse correlation exists Between stefin A level and malignant progression. The aim of this study is to investigate the role of stefin A in human esophageal squamous cell carcinoma cells and to evaluate the possiBility of stefin A for cancer therapy. Experimental Design: We staBly transfected stefin A cDNA into human EC9706 or KYSE150 esophageal squamous cell carcinoma cells. SuBsequently, we evaluated the effect of stefin A overexpression on cell growth, <B>CathepsinB> B activity, cell motility and invasion, tumor growth, and metastasis. Immunoanalysis was done to assess the expression of factor VIII and to support the localization of stefin A and <B>CathepsinB> B. We also evaluated the effect of CA074Me, a selective memBrane-permeant <B>CathepsinB> B inhiBitor. Results: Both transfection of stefin A and treatment with 10 μmol/L CA074Me significantly reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. ComBination of Both further reduced <B>CathepsinB> B activity and inhiBited the Matrigel invasion. Overexpression of stefin A delayed the in vitro and in vivo growth of cells and significantly inhiBited lung metastasis compared with 50% of lung metastasis in xenograft mice from EC9706 or empty vector cells. Transfection with stefin A showed a dramatic reduction of factor VIII staining in the tumors of xenograft mice. Conclusions: Our data strongly indicate that stefin A plays an important role in the growth, angiogenesis, invasion, and metastasis of human esophageal squamous cell carcinoma cells and suggest that stefin A may Be useful in cancer therapy.