The Experts below are selected from a list of 315 Experts worldwide ranked by ideXlab platform
Qiongxin Wang - One of the best experts on this subject based on the ideXlab platform.
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gefitinib mediated reactive Oxygen Specie ros instigates mitochondrial dysfunction and drug resistance in lung cancer cells
Journal of Biological Chemistry, 2015Co-Authors: Imoh S Okon, Kathleen A Coughlan, Miao Zhang, Qiongxin WangAbstract:Therapeutic benefits offered by tyrosine kinase inhibitors (TKIs), such as gefitinib (Iressa) and erlotinib (Tarceva) are limited due to the development of resistance which contributes to treatment failure and cancerrelated mortality. The aim of this study was to elucidate mechanistic insight on cellular perturbations that accompany acquired gefitinib resistance in lung cancer cells. Several lung adenocarcinoma (LAD) cell lines were screened to characterize EGFR expression and mutation profile. In order to circumvent intrinsic variations between cell lines with respect to response to drug treatments, we generated gefitinib-resistant H1650 clone by long-term, chronic culture under gefitinib selection of parental cell line. Isogenic cells
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Gefitinib-mediated Reactive Oxygen Specie (ROS) Instigates Mitochondrial Dysfunction and Drug Resistance in Lung Cancer Cells
The Journal of biological chemistry, 2015Co-Authors: Imoh Okon, Kathleen A Coughlan, Miao Zhang, Qiongxin Wang, Ming-hui ZouAbstract:Therapeutic benefits offered by tyrosine kinase inhibitors (TKIs), such as gefitinib (Iressa) and erlotinib (Tarceva), are limited due to the development of resistance, which contributes to treatment failure and cancer-related mortality. The aim of this study was to elucidate mechanistic insight into cellular perturbations that accompany acquired gefitinib resistance in lung cancer cells. Several lung adenocarcinoma (LAD) cell lines were screened to characterize epidermal growth factor receptor (EGFR) expression and mutation profile. To circumvent intrinsic variations between cell lines with respect to response to drug treatments, we generated gefitinib-resistant H1650 clone by long-term, chronic culture under gefitinib selection of parental cell line. Isogenic cells were analyzed by microarray, Western blot, flow cytometry, and confocal and transmission electron microscope. We observed that although chronic gefitinib treatment provided effective action against its primary target (aberrant EGFR activity), secondary effects resulted in increased cellular reactive Oxygen Species (ROS). Gefitinib-mediated ROS correlated with epithelial-mesenchymal transition, as well as striking perturbation of mitochondrial morphology and function. However, gefitinib treatment in the presence of ROS scavenger provided a partial rescue of mitochondrial aberrations. Furthermore, withdrawal of gefitinib from previously resistant clones correlated with normalized expression of epithelial-mesenchymal transition genes. These findings demonstrate that chronic gefitinib treatment promotes ROS and mitochondrial dysfunction in lung cancer cells. Antioxidants may alleviate ROS-mediated resistance.
Ming-hui Zou - One of the best experts on this subject based on the ideXlab platform.
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Gefitinib-mediated Reactive Oxygen Specie (ROS) Instigates Mitochondrial Dysfunction and Drug Resistance in Lung Cancer Cells
The Journal of biological chemistry, 2015Co-Authors: Imoh Okon, Kathleen A Coughlan, Miao Zhang, Qiongxin Wang, Ming-hui ZouAbstract:Therapeutic benefits offered by tyrosine kinase inhibitors (TKIs), such as gefitinib (Iressa) and erlotinib (Tarceva), are limited due to the development of resistance, which contributes to treatment failure and cancer-related mortality. The aim of this study was to elucidate mechanistic insight into cellular perturbations that accompany acquired gefitinib resistance in lung cancer cells. Several lung adenocarcinoma (LAD) cell lines were screened to characterize epidermal growth factor receptor (EGFR) expression and mutation profile. To circumvent intrinsic variations between cell lines with respect to response to drug treatments, we generated gefitinib-resistant H1650 clone by long-term, chronic culture under gefitinib selection of parental cell line. Isogenic cells were analyzed by microarray, Western blot, flow cytometry, and confocal and transmission electron microscope. We observed that although chronic gefitinib treatment provided effective action against its primary target (aberrant EGFR activity), secondary effects resulted in increased cellular reactive Oxygen Species (ROS). Gefitinib-mediated ROS correlated with epithelial-mesenchymal transition, as well as striking perturbation of mitochondrial morphology and function. However, gefitinib treatment in the presence of ROS scavenger provided a partial rescue of mitochondrial aberrations. Furthermore, withdrawal of gefitinib from previously resistant clones correlated with normalized expression of epithelial-mesenchymal transition genes. These findings demonstrate that chronic gefitinib treatment promotes ROS and mitochondrial dysfunction in lung cancer cells. Antioxidants may alleviate ROS-mediated resistance.
Kathleen A Coughlan - One of the best experts on this subject based on the ideXlab platform.
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gefitinib mediated reactive Oxygen Specie ros instigates mitochondrial dysfunction and drug resistance in lung cancer cells
Journal of Biological Chemistry, 2015Co-Authors: Imoh S Okon, Kathleen A Coughlan, Miao Zhang, Qiongxin WangAbstract:Therapeutic benefits offered by tyrosine kinase inhibitors (TKIs), such as gefitinib (Iressa) and erlotinib (Tarceva) are limited due to the development of resistance which contributes to treatment failure and cancerrelated mortality. The aim of this study was to elucidate mechanistic insight on cellular perturbations that accompany acquired gefitinib resistance in lung cancer cells. Several lung adenocarcinoma (LAD) cell lines were screened to characterize EGFR expression and mutation profile. In order to circumvent intrinsic variations between cell lines with respect to response to drug treatments, we generated gefitinib-resistant H1650 clone by long-term, chronic culture under gefitinib selection of parental cell line. Isogenic cells
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Gefitinib-mediated Reactive Oxygen Specie (ROS) Instigates Mitochondrial Dysfunction and Drug Resistance in Lung Cancer Cells
The Journal of biological chemistry, 2015Co-Authors: Imoh Okon, Kathleen A Coughlan, Miao Zhang, Qiongxin Wang, Ming-hui ZouAbstract:Therapeutic benefits offered by tyrosine kinase inhibitors (TKIs), such as gefitinib (Iressa) and erlotinib (Tarceva), are limited due to the development of resistance, which contributes to treatment failure and cancer-related mortality. The aim of this study was to elucidate mechanistic insight into cellular perturbations that accompany acquired gefitinib resistance in lung cancer cells. Several lung adenocarcinoma (LAD) cell lines were screened to characterize epidermal growth factor receptor (EGFR) expression and mutation profile. To circumvent intrinsic variations between cell lines with respect to response to drug treatments, we generated gefitinib-resistant H1650 clone by long-term, chronic culture under gefitinib selection of parental cell line. Isogenic cells were analyzed by microarray, Western blot, flow cytometry, and confocal and transmission electron microscope. We observed that although chronic gefitinib treatment provided effective action against its primary target (aberrant EGFR activity), secondary effects resulted in increased cellular reactive Oxygen Species (ROS). Gefitinib-mediated ROS correlated with epithelial-mesenchymal transition, as well as striking perturbation of mitochondrial morphology and function. However, gefitinib treatment in the presence of ROS scavenger provided a partial rescue of mitochondrial aberrations. Furthermore, withdrawal of gefitinib from previously resistant clones correlated with normalized expression of epithelial-mesenchymal transition genes. These findings demonstrate that chronic gefitinib treatment promotes ROS and mitochondrial dysfunction in lung cancer cells. Antioxidants may alleviate ROS-mediated resistance.
Miao Zhang - One of the best experts on this subject based on the ideXlab platform.
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gefitinib mediated reactive Oxygen Specie ros instigates mitochondrial dysfunction and drug resistance in lung cancer cells
Journal of Biological Chemistry, 2015Co-Authors: Imoh S Okon, Kathleen A Coughlan, Miao Zhang, Qiongxin WangAbstract:Therapeutic benefits offered by tyrosine kinase inhibitors (TKIs), such as gefitinib (Iressa) and erlotinib (Tarceva) are limited due to the development of resistance which contributes to treatment failure and cancerrelated mortality. The aim of this study was to elucidate mechanistic insight on cellular perturbations that accompany acquired gefitinib resistance in lung cancer cells. Several lung adenocarcinoma (LAD) cell lines were screened to characterize EGFR expression and mutation profile. In order to circumvent intrinsic variations between cell lines with respect to response to drug treatments, we generated gefitinib-resistant H1650 clone by long-term, chronic culture under gefitinib selection of parental cell line. Isogenic cells
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Gefitinib-mediated Reactive Oxygen Specie (ROS) Instigates Mitochondrial Dysfunction and Drug Resistance in Lung Cancer Cells
The Journal of biological chemistry, 2015Co-Authors: Imoh Okon, Kathleen A Coughlan, Miao Zhang, Qiongxin Wang, Ming-hui ZouAbstract:Therapeutic benefits offered by tyrosine kinase inhibitors (TKIs), such as gefitinib (Iressa) and erlotinib (Tarceva), are limited due to the development of resistance, which contributes to treatment failure and cancer-related mortality. The aim of this study was to elucidate mechanistic insight into cellular perturbations that accompany acquired gefitinib resistance in lung cancer cells. Several lung adenocarcinoma (LAD) cell lines were screened to characterize epidermal growth factor receptor (EGFR) expression and mutation profile. To circumvent intrinsic variations between cell lines with respect to response to drug treatments, we generated gefitinib-resistant H1650 clone by long-term, chronic culture under gefitinib selection of parental cell line. Isogenic cells were analyzed by microarray, Western blot, flow cytometry, and confocal and transmission electron microscope. We observed that although chronic gefitinib treatment provided effective action against its primary target (aberrant EGFR activity), secondary effects resulted in increased cellular reactive Oxygen Species (ROS). Gefitinib-mediated ROS correlated with epithelial-mesenchymal transition, as well as striking perturbation of mitochondrial morphology and function. However, gefitinib treatment in the presence of ROS scavenger provided a partial rescue of mitochondrial aberrations. Furthermore, withdrawal of gefitinib from previously resistant clones correlated with normalized expression of epithelial-mesenchymal transition genes. These findings demonstrate that chronic gefitinib treatment promotes ROS and mitochondrial dysfunction in lung cancer cells. Antioxidants may alleviate ROS-mediated resistance.
Feng Bin - One of the best experts on this subject based on the ideXlab platform.
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Catalytic self-sustained combustion of toluene and reaction pathway over CuxMn1-xCe0.75Zr0.25/TiO2 catalysts
Applied Catalysis A: General, 2019Co-Authors: Chenchen Zhao, Qinglan Hao, Qing Zhang, Ningna Yan, Jiaren Liu, Baojuan Dou, Feng BinAbstract:Abstract The catalytic self-sustained combustion of toluene over CuxMn1-xCe0.75Zr0.25/TiO2 catalysts (x = 1, 0.5, 0) was studied in a microscale combustor. The catalytic activity is determined not only by the temperature with toluene conversion of 90% (Tco), but also by the corresponding lean-combustion limits. It was found that the self-sustained combustion was achieved successfully over the catalysts, with the toluene concentrations of 0.35 con.%, 0.50 con.% and 1.00 con.%. According to Tco, the activity decreased in the order of CuCe0.75Zr0.25/TiO2 (234 °C)＞Cu0.5Mn0.5Ce0.75Zr0.25/TiO2 (238 °C) ＞MnCe0.75Zr0.25/TiO2 (284 °C). The excellent activity of CuCe0.75Zr0.25/TiO2 catalyst could be ascribed to the high content of active lattice Oxygen, good low-temperature reducibility and homogeneous dispersion, combined with the results of H2-TPR, O2-TPD and XPS. Furthermore, the results of in-situ DRIFT and temperature-programmed oxidation (TPO) of toluene in N2 atmosphere suggested that toluene was adsorbed on the catalyst surface by removing α-H from methyl and combining with active Oxygen Specie to form benzyl group, which was finally oxidized into CO2 and H2O with lattice Oxygen.
