The Experts below are selected from a list of 5313 Experts worldwide ranked by ideXlab platform
Jia Luo - One of the best experts on this subject based on the ideXlab platform.
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Cyanidin 3 Glucoside ameliorates ethanol neurotoxicity in the developing brain
Journal of Neuroscience Research, 2011Co-Authors: Ying Liu, X Wang, Gang Chen, Kimberly A Bower, Xianglin Shi, Jacqueline A Frank, Zhiqin Fan, Jia LuoAbstract:Ethanol exposure induces neurodegeneration in the developing central nervous system (CNS). Fetal Alcohol Spectrum Disorders (FASD) are caused by ethanol exposure during pregnancy and are the most common nonhereditary cause of mental retardation. It is important to identify agents that provide neuroprotection against ethanol neurotoxicity. Multiple mechanisms have been proposed for ethanol-induced neurodegeneration, and oxidative stress is one of the most important mechanisms. Recent evidence indicates that glycogen synthase kinase 3β (GSK3β) is a potential mediator of ethanol-mediated neuronal death (Luo, 2009). Cyanidin-3-Glucoside (C3G), a member of the anthocyanin family, is a potent natural antioxidant. Our previous study suggested that C3G inhibited GSK3β activity in neurons (Chen et al., 2009). Using a third trimester equivalent mouse model of ethanol exposure, we tested the hypothesis that C3G can ameliorate ethanol-induced neuronal death in the developing brain. Intraperitoneal injection of C3G reduced ethanol-meditated caspase-3 activation, neurodegeneration and microglial activation in the cerebral cortex of seven-day-old mice. C3G blocked ethanol-mediated GSK3β activation by inducing the phosphorylation at serine 9 while reducing the phosphorylation at tyrosine 216. C3G also inhibited ethanol-stimulated expression of malondialdehyde (MDA) and p47phox, indicating that C3G alleviated ethanol-induced oxidative stress. These results provide important insight into the therapeutic potential of C3G.
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Cyanidin 3 Glucoside ameliorates ethanol neurotoxicity in the developing brain
Journal of Neuroscience Research, 2011Co-Authors: Ying Liu, Gang Chen, Kimberly A Bower, Xianglin Shi, Jacqueline A Frank, Zhiqin Fan, Xin Wang, Jia LuoAbstract:Ethanol exposure induces neurodegeneration in the developing central nervous system (CNS). Fetal alcohol spectrum disorders (FASD) are caused by ethanol exposure during pregnancy and are the most common nonhereditary cause of mental retardation. It is important to identify agents that provide neuroprotection against ethanol neurotoxicity. Multiple mechanisms have been proposed for ethanol-induced neurodegeneration, and oxidative stress is one of the most important mechanisms. Recent evidence indicates that glycogen synthase kinase 3β (GSK3β) is a potential mediator of ethanol-mediated neuronal death. Cyanidin-3-Glucoside (C3G), a member of the anthocyanin family, is a potent natural antioxidant. Our previous study suggested that C3G inhibited GSK3β activity in neurons. Using a third trimester equivalent mouse model of ethanol exposure, we tested the hypothesis that C3G can ameliorate ethanol-induced neuronal death in the developing brain. Intraperitoneal injection of C3G reduced ethanol-meditated caspase-3 activation, neurodegeneration, and microglial activation in the cerebral cortex of 7-day-old mice. C3G blocked ethanol-mediated GSK3β activation by inducing phosphorylation at serine 9 while reducing the phosphorylation at tyrosine 216. C3G also inhibited ethanol-stimulated expression of malondialdehyde (MDA) and p47phox, indicating that C3G alleviated ethanol-induced oxidative stress. These results provide important insight into the therapeutic potential of C3G.
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Cyanidin 3 Glucoside inhibits ethanol induced invasion of breast cancer cells overexpressing erbb2
Molecular Cancer, 2010Co-Authors: Kimberly A Bower, Gang Chen, Min Ding, Xianglin Shi, Siying Wang, Jacqueline A Frank, Shiow Wang, Jia LuoAbstract:Background Ethanol is a tumor promoter. Both epidemiological and experimental studies suggest that ethanol may enhance the metastasis of breast cancer cells. We have previously demonstrated that ethanol increased the migration/invasion of breast cancer cells expressing high levels of ErbB2. Amplification of ErbB2 is found in 20-30% of breast cancer patients and is associated with poor prognosis. We sought to identify agents that can prevent or ameliorate ethanol-induced invasion of breast cancer cells. Cyanidin-3-Glucoside (C3G), an anthocyanin present in many vegetables and fruits, is a potent natural antioxidant. Ethanol exposure causes the accumulation of intracellular reactive oxygen species (ROS). This study evaluated the effect of C3G on ethanol-induced breast cancer cell migration/invasion.
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Cyanidin 3 Glucoside inhibits ethanol induced invasion of breast cancer cells overexpressing erbb2
Molecular Cancer, 2010Co-Authors: Kimberly A Bower, Gang Chen, Min Ding, Xianglin Shi, Siying Wang, Jacqueline A Frank, Shiow Wang, Jia LuoAbstract:Ethanol is a tumor promoter. Both epidemiological and experimental studies suggest that ethanol may enhance the metastasis of breast cancer cells. We have previously demonstrated that ethanol increased the migration/invasion of breast cancer cells expressing high levels of ErbB2. Amplification of ErbB2 is found in 20-30% of breast cancer patients and is associated with poor prognosis. We sought to identify agents that can prevent or ameliorate ethanol-induced invasion of breast cancer cells. Cyanidin-3-Glucoside (C3G), an anthocyanin present in many vegetables and fruits, is a potent natural antioxidant. Ethanol exposure causes the accumulation of intracellular reactive oxygen species (ROS). This study evaluated the effect of C3G on ethanol-induced breast cancer cell migration/invasion. C3G attenuated ethanol-induced migration/invasion of breast cancer cells expressing high levels of ErbB2 (BT474, MDA-MB231 and MCF7ErbB2) in a concentration dependent manner. C3G decreased ethanol-mediated cell adhesion to the extracellular matrix (ECM) as well as the amount of focal adhesions and the formation of lamellipodial protrusion. It inhibited ethanol-stimulated phosphorylation of ErbB2, cSrc, FAK and p130Cas, as well as interactions among these proteins. C3G abolished ethanol-mediated p130Cas/JNK interaction. C3G blocks ethanol-induced activation of the ErbB2/cSrc/FAK pathway which is necessary for cell migration/invasion. C3G may be beneficial in preventing/reducing ethanol-induced breast cancer metastasis.
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Cyanidin 3 Glucoside reverses ethanol induced inhibition of neurite outgrowth role of glycogen synthase kinase 3 beta
Neurotoxicity Research, 2009Co-Authors: Gang Chen, Kimberly A Bower, Min Ding, Xianglin Shi, Jia LuoAbstract:Ethanol is a potent teratogen for the developing central nervous system (CNS), and fetal alcohol syndrome (FAS) is the most common nonhereditary cause of mental retardation. Ethanol disrupts neuronal differentiation and maturation. It is important to identify agents that provide neuroprotection against ethanol neurotoxicity. Using an in vitro neuronal model, mouse Neuro2a (N2a) neuroblastoma cells, we demonstrated that ethanol inhibited neurite outgrowth and the expression of neurofilament (NF) proteins. Glycogen synthase kinase 3β (GSK3β), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3β activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3β mutant prevented neurite outgrowth. Ethanol inhibited neurite outgrowth by activating GSK3β through the dephosphorylation of GSK3β at serine 9. Cyanidin-3-Glucoside (C3G), a member of the anthocyanin family rich in many edible berries and other pigmented fruits, enhanced neurite outgrowth by promoting p-GSK3β(Ser9). More importantly, C3G reversed ethanol-mediated activation of GSK3β and inhibition of neurite outgrowth as well as the expression of NF proteins. C3G also blocked ethanol-induced intracellular accumulation of reactive oxygen species (ROS). However, the antioxidant effect of C3G appeared minimally involved in its protection. Our study provides a potential avenue for preventing or ameliorating ethanol-induced damage to the developing CNS.
Yihshou Hsieh - One of the best experts on this subject based on the ideXlab platform.
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mulberry anthocyanins Cyanidin 3 rutinoside and Cyanidin 3 Glucoside exhibited an inhibitory effect on the migration and invasion of a human lung cancer cell line
Cancer Letters, 2006Co-Authors: Peini Chen, Shuchen Chu, Huiling Chiou, Chuiliang Chiang, Wuhsien Kuo, Yihshou HsiehAbstract:Anthocyanins, present in various fruits and vegetables as natural colorant, have been well characterized to be involved in various bioactive properties and are wildly used for their antioxidant properties. Furthermore, recent studies have revealed pleiotropic anticancer and antiproliferative capabilities of anthocyanin. Berry extract contains high amounts of anthocyanins and is commonly used in diet or in some therapeutic applications. In this study, we first observed that Cyanidin 3-rutinoside and Cyanidin 3-Glucoside (extracted from Morus alba L.) exerted a dose-dependent inhibitory effect on the migration and invasion, of highly metastatic A549 human lung carcinoma cells in absence of cytotoxicity. The results showed that Cyanidin 3-Glucoside and Cyanidin 3-rutinoside treatments could decrease the expressions of matrix matalloprotinase-2 (MMP-2) and urokinase-plasminogen activator (u-PA) in a dose-dependent manner and enhance the expression of tissue inhibitor of matrix matalloprotinase-2 (TIMP-2) and plasminogen activator inhibitor (PAI). Further analysis with semi-quantitative RT-PCR showed that these alterations were all on the transcriptional level. Further, a treatment of Cyanidin 3-rutinoside and Cyanidin 3-Glucoside also resulted in an inhibition on the activation of c-Jun and NF-kappaB. Together, these result suggested that anthocyanins could decrease the in vitro invasiveness of cancer cells and therefore, may be of great value in developing a potential cancer therapy.
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Cyanidin 3 Glucoside and peonidin 3 Glucoside inhibit tumor cell growth and induce apoptosis in vitro and suppress tumor growth in vivo
Nutrition and Cancer, 2005Co-Authors: Peini Chen, Shuchen Chu, Huiling Chiou, Chuiliang Chiang, Shunfa Yang, Yihshou HsiehAbstract:Abstract: Dietary polyphenols, including anthocyanins, are suggested to be involved in the protective effects of fruits and vegetables against cancer. However, anticancer effects of peonidin 3-Glucoside have not been clearly demonstrated, with only limited studies being available concerning the inhibitory effect of Cyanidin 3-Glucoside for tumor cell growth. Therefore, in this study, we have isolated and identified the two bioactive compounds, peonidin 3-Glucoside and Cyanidin 3-Glucoside, from Oryza sativa L. indica, to treat various cancer cells. The results showed that, among analyzed cell lines, HS578T was the most sensitive to peonidin 3-Glucoside and Cyanidin 3-Glucoside. Treatment with peonidin 3-Glucoside or Cyanidin 3-Glucoside resulted in a strong inhibitory effect on cell growth via G2/M arrest. Regarding cell cycle–related proteins, peonidin 3-Glucoside treatment resulted in down-regulation of protein levels of cyclin-dependent kinase (CDK)-1, CDK-2, cyclin B1, and cyclin E, whereas Cyanidin 3...
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Cyanidin 3-Glucoside and peonidin 3-Glucoside inhibit tumor cell growth and induce apoptosis in vitro and suppress tumor growth in vivo.
Nutrition and Cancer, 2005Co-Authors: Peini Chen, Shuchen Chu, Huiling Chiou, Chuiliang Chiang, Shunfa Yang, Yihshou HsiehAbstract:Dietary polyphenols, including anthocyanins, are suggested to be involved in the protective effects of fruits and vegetables against cancer. However, anticancer effects of peonidin 3-Glucoside have not been clearly demonstrated, with only limited studies being available concerning the inhibitory effect of Cyanidin 3-Glucoside for tumor cell growth. Therefore, in this study, we have isolated and identified the two bioactive compounds, peonidin 3-Glucoside and Cyanidin 3-Glucoside, from Oryza sativa L. indica, to treat various cancer cells. The results showed that, among analyzed cell lines, HS578T was the most sensitive to peonidin 3-Glucoside and Cyanidin 3-Glucoside. Treatment with peonidin 3-Glucoside or Cyanidin 3-Glucoside resulted in a strong inhibitory effect on cell growth via G2/M arrest. Regarding cell cyclerelated proteins, peonidin 3-Glucoside treatment resulted in down-regulation of protein levels of cyclin-dependent kinase (CDK)-1, CDK-2, cyclin B1, and cyclin E, whereas Cyanidin 3-Glucoside could decrease the protein levels of CDK-1, CDK-2, cyclin B1, and cyclin D1. In addition, Cyanidin 3-Glucoside or peonidin 3-Glucoside also induced caspase-3 activation, chromatin condensation, and cell death. Furthermore, anthocyanins from O. sativa L. indica were evidenced by their inhibition on the growth of Lewis lung carcinoma cells in vivo.
Xianglin Shi - One of the best experts on this subject based on the ideXlab platform.
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Cyanidin 3 Glucoside ameliorates ethanol neurotoxicity in the developing brain
Journal of Neuroscience Research, 2011Co-Authors: Ying Liu, X Wang, Gang Chen, Kimberly A Bower, Xianglin Shi, Jacqueline A Frank, Zhiqin Fan, Jia LuoAbstract:Ethanol exposure induces neurodegeneration in the developing central nervous system (CNS). Fetal Alcohol Spectrum Disorders (FASD) are caused by ethanol exposure during pregnancy and are the most common nonhereditary cause of mental retardation. It is important to identify agents that provide neuroprotection against ethanol neurotoxicity. Multiple mechanisms have been proposed for ethanol-induced neurodegeneration, and oxidative stress is one of the most important mechanisms. Recent evidence indicates that glycogen synthase kinase 3β (GSK3β) is a potential mediator of ethanol-mediated neuronal death (Luo, 2009). Cyanidin-3-Glucoside (C3G), a member of the anthocyanin family, is a potent natural antioxidant. Our previous study suggested that C3G inhibited GSK3β activity in neurons (Chen et al., 2009). Using a third trimester equivalent mouse model of ethanol exposure, we tested the hypothesis that C3G can ameliorate ethanol-induced neuronal death in the developing brain. Intraperitoneal injection of C3G reduced ethanol-meditated caspase-3 activation, neurodegeneration and microglial activation in the cerebral cortex of seven-day-old mice. C3G blocked ethanol-mediated GSK3β activation by inducing the phosphorylation at serine 9 while reducing the phosphorylation at tyrosine 216. C3G also inhibited ethanol-stimulated expression of malondialdehyde (MDA) and p47phox, indicating that C3G alleviated ethanol-induced oxidative stress. These results provide important insight into the therapeutic potential of C3G.
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Cyanidin 3 Glucoside ameliorates ethanol neurotoxicity in the developing brain
Journal of Neuroscience Research, 2011Co-Authors: Ying Liu, Gang Chen, Kimberly A Bower, Xianglin Shi, Jacqueline A Frank, Zhiqin Fan, Xin Wang, Jia LuoAbstract:Ethanol exposure induces neurodegeneration in the developing central nervous system (CNS). Fetal alcohol spectrum disorders (FASD) are caused by ethanol exposure during pregnancy and are the most common nonhereditary cause of mental retardation. It is important to identify agents that provide neuroprotection against ethanol neurotoxicity. Multiple mechanisms have been proposed for ethanol-induced neurodegeneration, and oxidative stress is one of the most important mechanisms. Recent evidence indicates that glycogen synthase kinase 3β (GSK3β) is a potential mediator of ethanol-mediated neuronal death. Cyanidin-3-Glucoside (C3G), a member of the anthocyanin family, is a potent natural antioxidant. Our previous study suggested that C3G inhibited GSK3β activity in neurons. Using a third trimester equivalent mouse model of ethanol exposure, we tested the hypothesis that C3G can ameliorate ethanol-induced neuronal death in the developing brain. Intraperitoneal injection of C3G reduced ethanol-meditated caspase-3 activation, neurodegeneration, and microglial activation in the cerebral cortex of 7-day-old mice. C3G blocked ethanol-mediated GSK3β activation by inducing phosphorylation at serine 9 while reducing the phosphorylation at tyrosine 216. C3G also inhibited ethanol-stimulated expression of malondialdehyde (MDA) and p47phox, indicating that C3G alleviated ethanol-induced oxidative stress. These results provide important insight into the therapeutic potential of C3G.
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Cyanidin 3 Glucoside inhibits ethanol induced invasion of breast cancer cells overexpressing erbb2
Molecular Cancer, 2010Co-Authors: Kimberly A Bower, Gang Chen, Min Ding, Xianglin Shi, Siying Wang, Jacqueline A Frank, Shiow Wang, Jia LuoAbstract:Background Ethanol is a tumor promoter. Both epidemiological and experimental studies suggest that ethanol may enhance the metastasis of breast cancer cells. We have previously demonstrated that ethanol increased the migration/invasion of breast cancer cells expressing high levels of ErbB2. Amplification of ErbB2 is found in 20-30% of breast cancer patients and is associated with poor prognosis. We sought to identify agents that can prevent or ameliorate ethanol-induced invasion of breast cancer cells. Cyanidin-3-Glucoside (C3G), an anthocyanin present in many vegetables and fruits, is a potent natural antioxidant. Ethanol exposure causes the accumulation of intracellular reactive oxygen species (ROS). This study evaluated the effect of C3G on ethanol-induced breast cancer cell migration/invasion.
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Cyanidin 3 Glucoside inhibits ethanol induced invasion of breast cancer cells overexpressing erbb2
Molecular Cancer, 2010Co-Authors: Kimberly A Bower, Gang Chen, Min Ding, Xianglin Shi, Siying Wang, Jacqueline A Frank, Shiow Wang, Jia LuoAbstract:Ethanol is a tumor promoter. Both epidemiological and experimental studies suggest that ethanol may enhance the metastasis of breast cancer cells. We have previously demonstrated that ethanol increased the migration/invasion of breast cancer cells expressing high levels of ErbB2. Amplification of ErbB2 is found in 20-30% of breast cancer patients and is associated with poor prognosis. We sought to identify agents that can prevent or ameliorate ethanol-induced invasion of breast cancer cells. Cyanidin-3-Glucoside (C3G), an anthocyanin present in many vegetables and fruits, is a potent natural antioxidant. Ethanol exposure causes the accumulation of intracellular reactive oxygen species (ROS). This study evaluated the effect of C3G on ethanol-induced breast cancer cell migration/invasion. C3G attenuated ethanol-induced migration/invasion of breast cancer cells expressing high levels of ErbB2 (BT474, MDA-MB231 and MCF7ErbB2) in a concentration dependent manner. C3G decreased ethanol-mediated cell adhesion to the extracellular matrix (ECM) as well as the amount of focal adhesions and the formation of lamellipodial protrusion. It inhibited ethanol-stimulated phosphorylation of ErbB2, cSrc, FAK and p130Cas, as well as interactions among these proteins. C3G abolished ethanol-mediated p130Cas/JNK interaction. C3G blocks ethanol-induced activation of the ErbB2/cSrc/FAK pathway which is necessary for cell migration/invasion. C3G may be beneficial in preventing/reducing ethanol-induced breast cancer metastasis.
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Cyanidin 3 Glucoside reverses ethanol induced inhibition of neurite outgrowth role of glycogen synthase kinase 3 beta
Neurotoxicity Research, 2009Co-Authors: Gang Chen, Kimberly A Bower, Min Ding, Xianglin Shi, Jia LuoAbstract:Ethanol is a potent teratogen for the developing central nervous system (CNS), and fetal alcohol syndrome (FAS) is the most common nonhereditary cause of mental retardation. Ethanol disrupts neuronal differentiation and maturation. It is important to identify agents that provide neuroprotection against ethanol neurotoxicity. Using an in vitro neuronal model, mouse Neuro2a (N2a) neuroblastoma cells, we demonstrated that ethanol inhibited neurite outgrowth and the expression of neurofilament (NF) proteins. Glycogen synthase kinase 3β (GSK3β), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3β activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3β mutant prevented neurite outgrowth. Ethanol inhibited neurite outgrowth by activating GSK3β through the dephosphorylation of GSK3β at serine 9. Cyanidin-3-Glucoside (C3G), a member of the anthocyanin family rich in many edible berries and other pigmented fruits, enhanced neurite outgrowth by promoting p-GSK3β(Ser9). More importantly, C3G reversed ethanol-mediated activation of GSK3β and inhibition of neurite outgrowth as well as the expression of NF proteins. C3G also blocked ethanol-induced intracellular accumulation of reactive oxygen species (ROS). However, the antioxidant effect of C3G appeared minimally involved in its protection. Our study provides a potential avenue for preventing or ameliorating ethanol-induced damage to the developing CNS.
Min Ding - One of the best experts on this subject based on the ideXlab platform.
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Cyanidin 3 Glucoside inhibits ethanol induced invasion of breast cancer cells overexpressing erbb2
Molecular Cancer, 2010Co-Authors: Kimberly A Bower, Gang Chen, Min Ding, Xianglin Shi, Siying Wang, Jacqueline A Frank, Shiow Wang, Jia LuoAbstract:Ethanol is a tumor promoter. Both epidemiological and experimental studies suggest that ethanol may enhance the metastasis of breast cancer cells. We have previously demonstrated that ethanol increased the migration/invasion of breast cancer cells expressing high levels of ErbB2. Amplification of ErbB2 is found in 20-30% of breast cancer patients and is associated with poor prognosis. We sought to identify agents that can prevent or ameliorate ethanol-induced invasion of breast cancer cells. Cyanidin-3-Glucoside (C3G), an anthocyanin present in many vegetables and fruits, is a potent natural antioxidant. Ethanol exposure causes the accumulation of intracellular reactive oxygen species (ROS). This study evaluated the effect of C3G on ethanol-induced breast cancer cell migration/invasion. C3G attenuated ethanol-induced migration/invasion of breast cancer cells expressing high levels of ErbB2 (BT474, MDA-MB231 and MCF7ErbB2) in a concentration dependent manner. C3G decreased ethanol-mediated cell adhesion to the extracellular matrix (ECM) as well as the amount of focal adhesions and the formation of lamellipodial protrusion. It inhibited ethanol-stimulated phosphorylation of ErbB2, cSrc, FAK and p130Cas, as well as interactions among these proteins. C3G abolished ethanol-mediated p130Cas/JNK interaction. C3G blocks ethanol-induced activation of the ErbB2/cSrc/FAK pathway which is necessary for cell migration/invasion. C3G may be beneficial in preventing/reducing ethanol-induced breast cancer metastasis.
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Cyanidin 3 Glucoside inhibits ethanol induced invasion of breast cancer cells overexpressing erbb2
Molecular Cancer, 2010Co-Authors: Kimberly A Bower, Gang Chen, Min Ding, Xianglin Shi, Siying Wang, Jacqueline A Frank, Shiow Wang, Jia LuoAbstract:Background Ethanol is a tumor promoter. Both epidemiological and experimental studies suggest that ethanol may enhance the metastasis of breast cancer cells. We have previously demonstrated that ethanol increased the migration/invasion of breast cancer cells expressing high levels of ErbB2. Amplification of ErbB2 is found in 20-30% of breast cancer patients and is associated with poor prognosis. We sought to identify agents that can prevent or ameliorate ethanol-induced invasion of breast cancer cells. Cyanidin-3-Glucoside (C3G), an anthocyanin present in many vegetables and fruits, is a potent natural antioxidant. Ethanol exposure causes the accumulation of intracellular reactive oxygen species (ROS). This study evaluated the effect of C3G on ethanol-induced breast cancer cell migration/invasion.
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Cyanidin 3 Glucoside reverses ethanol induced inhibition of neurite outgrowth role of glycogen synthase kinase 3 beta
Neurotoxicity Research, 2009Co-Authors: Gang Chen, Kimberly A Bower, Min Ding, Xianglin Shi, Jia LuoAbstract:Ethanol is a potent teratogen for the developing central nervous system (CNS), and fetal alcohol syndrome (FAS) is the most common nonhereditary cause of mental retardation. Ethanol disrupts neuronal differentiation and maturation. It is important to identify agents that provide neuroprotection against ethanol neurotoxicity. Using an in vitro neuronal model, mouse Neuro2a (N2a) neuroblastoma cells, we demonstrated that ethanol inhibited neurite outgrowth and the expression of neurofilament (NF) proteins. Glycogen synthase kinase 3β (GSK3β), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3β activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3β mutant prevented neurite outgrowth. Ethanol inhibited neurite outgrowth by activating GSK3β through the dephosphorylation of GSK3β at serine 9. Cyanidin-3-Glucoside (C3G), a member of the anthocyanin family rich in many edible berries and other pigmented fruits, enhanced neurite outgrowth by promoting p-GSK3β(Ser9). More importantly, C3G reversed ethanol-mediated activation of GSK3β and inhibition of neurite outgrowth as well as the expression of NF proteins. C3G also blocked ethanol-induced intracellular accumulation of reactive oxygen species (ROS). However, the antioxidant effect of C3G appeared minimally involved in its protection. Our study provides a potential avenue for preventing or ameliorating ethanol-induced damage to the developing CNS.
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Cyanidin 3 Glucoside a natural product derived from blackberry exhibits chemopreventive and chemotherapeutic activity
Journal of Biological Chemistry, 2006Co-Authors: Min Ding, Shiow Y Wang, Rentian Feng, Linda Bowman, Yong Qian, Vincent Castranova, Binghua Jiang, Xianglin ShiAbstract:Epidemiological data suggest that consumption of fruits and vegetables has been associated with a lower incidence of cancer. Cyanidin-3-Glucoside (C3G), a compound found in blackberry and other food products, was shown to possess chemopreventive and chemotherapeutic activity in the present study. In cultured JB6 cells, C3G was able to scavenge ultraviolet B-induced OH and O2 . radicals. In vivo studies indicated that C3G treatment decreased the number of non-malignant and malignant skin tumors per mouse induced by 12-O-tetradecanolyphorbol-13-acetate (TPA) in 7,12-dimethylbenz[a]anthracene-initiated mouse skin. Pretreatment of JB6 cells with C3G inhibited UVB- and TPA-induced transactivation of NF-B and AP-1 and expression of cyclooxygenase-2 and tumor necrosis factor-. These inhibitory effects appear to be mediated through the inhibition of MAPK activity. C3G also blocked TPAinduced neoplastic transformation in JB6 cells. In addition, C3G inhibited proliferation of a human lung carcinoma cell line, A549. Animal studies showed that C3G reduced the size of A549 tumor xenograft growth and significantly inhibited metastasis in nude mice. Mechanistic studies indicated that C3G inhibited migration and invasion of A549 tumor cells. These finding demonstrate for the first time that a purified compound of anthocyanin inhibits tumor promoter-induced carcinogenesis and tumor metastasis in vivo.
Siying Wang - One of the best experts on this subject based on the ideXlab platform.
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Cyanidin 3 Glucoside inhibits ethanol induced invasion of breast cancer cells overexpressing erbb2
Molecular Cancer, 2010Co-Authors: Kimberly A Bower, Gang Chen, Min Ding, Xianglin Shi, Siying Wang, Jacqueline A Frank, Shiow Wang, Jia LuoAbstract:Background Ethanol is a tumor promoter. Both epidemiological and experimental studies suggest that ethanol may enhance the metastasis of breast cancer cells. We have previously demonstrated that ethanol increased the migration/invasion of breast cancer cells expressing high levels of ErbB2. Amplification of ErbB2 is found in 20-30% of breast cancer patients and is associated with poor prognosis. We sought to identify agents that can prevent or ameliorate ethanol-induced invasion of breast cancer cells. Cyanidin-3-Glucoside (C3G), an anthocyanin present in many vegetables and fruits, is a potent natural antioxidant. Ethanol exposure causes the accumulation of intracellular reactive oxygen species (ROS). This study evaluated the effect of C3G on ethanol-induced breast cancer cell migration/invasion.
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Cyanidin 3 Glucoside inhibits ethanol induced invasion of breast cancer cells overexpressing erbb2
Molecular Cancer, 2010Co-Authors: Kimberly A Bower, Gang Chen, Min Ding, Xianglin Shi, Siying Wang, Jacqueline A Frank, Shiow Wang, Jia LuoAbstract:Ethanol is a tumor promoter. Both epidemiological and experimental studies suggest that ethanol may enhance the metastasis of breast cancer cells. We have previously demonstrated that ethanol increased the migration/invasion of breast cancer cells expressing high levels of ErbB2. Amplification of ErbB2 is found in 20-30% of breast cancer patients and is associated with poor prognosis. We sought to identify agents that can prevent or ameliorate ethanol-induced invasion of breast cancer cells. Cyanidin-3-Glucoside (C3G), an anthocyanin present in many vegetables and fruits, is a potent natural antioxidant. Ethanol exposure causes the accumulation of intracellular reactive oxygen species (ROS). This study evaluated the effect of C3G on ethanol-induced breast cancer cell migration/invasion. C3G attenuated ethanol-induced migration/invasion of breast cancer cells expressing high levels of ErbB2 (BT474, MDA-MB231 and MCF7ErbB2) in a concentration dependent manner. C3G decreased ethanol-mediated cell adhesion to the extracellular matrix (ECM) as well as the amount of focal adhesions and the formation of lamellipodial protrusion. It inhibited ethanol-stimulated phosphorylation of ErbB2, cSrc, FAK and p130Cas, as well as interactions among these proteins. C3G abolished ethanol-mediated p130Cas/JNK interaction. C3G blocks ethanol-induced activation of the ErbB2/cSrc/FAK pathway which is necessary for cell migration/invasion. C3G may be beneficial in preventing/reducing ethanol-induced breast cancer metastasis.
