The Experts below are selected from a list of 87 Experts worldwide ranked by ideXlab platform
Hanming Shen - One of the best experts on this subject based on the ideXlab platform.
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chrysin sensitizes tumor necrosis factor α induced apoptosis in human tumor Cells via suppression of nuclear factor kappab
Cancer Letters, 2010Co-Authors: Xin Li, Qing Huang, Xingfen Yang, Hanming ShenAbstract:Abstract Chrysin (5,7-dihydroxyflavone) is a natural flavonoid commonly found in many plants. The anti-cancer property of chrysin has been demonstrated although the molecular mechanisms remain to be further elucidated. In the present study, we found that, pretreatment with chrysin greatly sensitized various human cancer Cells to tumor necrosis factor-alpha (TNFα)-induced apoptosis. In the search of the molecular mechanisms responsible for the sensitization effect of chrysin, we discovered that such sensitization is closely associated with the inhibitory effect of chrysin on TNFα-mediated nuclear transcription factor-kappaB (NF-κB) activation. Pretreatment with chrysin inhibited TNFα-induced degradation of Inhibitor of kappaB (IκB) protein and subsequent nuclear translocation of p65. As a result, chrysin suppressed the expression of NF-κB-targeted anti-apoptotic gene, c-FLIP-L. The role of c-FLIP-L was further confirmed by its ectopic expression, which significantly Protected Cell death induced by combined treatment with chrysin and TNFα. Data from this study thus reveal a novel function of chrysin and enhance the value of chrysin as an anti-cancer agent.
Hanming She - One of the best experts on this subject based on the ideXlab platform.
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luteolin sensitizes tumor necrosis factor α induced apoptosis in human tumor Cells
Oncogene, 2004Co-Authors: Ranxi Shi, Choon Nam Ong, Hanming SheAbstract:Tumor necrosis factor-α (TNFα) activates both Cell death and Cell survival pathways, which render most cancer Cells resistant to its cytotoxicity. In this study, we found that pretreatment with luteolin, a plant flavonoid, greatly sensitized TNFα-induced apoptotic Cell death in a number of human cancer Cell lines; including colorectal cancer COLO205, HCT116 Cells and cervical cancer HeLa Cells. In the search of the molecular mechanisms responsible for the sensitization effect of luteolin, we discovered that luteolin inhibited TNFα-induced activation of nuclear transcription factor-kappa B (NF-κB), the main survival factor in TNFα signaling. As a result, luteolin suppressed the expression of NF-κB-targeted antiapoptotic genes, including A20 and Cellular inhibitor of apoptosis protein-1 (c-IAP1). The role of A20 and c-IAP1 was further confirmed by ectopic expression of these two genes, which significantly Protected Cell death induced by luteolin followed by TNFα. In addition, inhibition of NF-κB by luteolin led to augmentation and prolongation of c-Jun N-terminal kinase (JNK) activation induced by TNFα. Suppression of JNK activation, either by a synthetic JNK inhibitor (SP600125) or by overexpression of the dominant negative forms of JNK kinase 1 (JNKK1) and JNK kinase 2 (JNKK2), conferred significant protection against apoptotic Cell death induced by luteolin and TNFα, suggesting that NF-κB and JNK are closely associated with the sensitization effect of luteolin. Data from this study reveal a novel function of luteolin and enhance the value of luteolin as an anticancer agent.
Xin Li - One of the best experts on this subject based on the ideXlab platform.
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chrysin sensitizes tumor necrosis factor α induced apoptosis in human tumor Cells via suppression of nuclear factor kappab
Cancer Letters, 2010Co-Authors: Xin Li, Qing Huang, Xingfen Yang, Hanming ShenAbstract:Abstract Chrysin (5,7-dihydroxyflavone) is a natural flavonoid commonly found in many plants. The anti-cancer property of chrysin has been demonstrated although the molecular mechanisms remain to be further elucidated. In the present study, we found that, pretreatment with chrysin greatly sensitized various human cancer Cells to tumor necrosis factor-alpha (TNFα)-induced apoptosis. In the search of the molecular mechanisms responsible for the sensitization effect of chrysin, we discovered that such sensitization is closely associated with the inhibitory effect of chrysin on TNFα-mediated nuclear transcription factor-kappaB (NF-κB) activation. Pretreatment with chrysin inhibited TNFα-induced degradation of Inhibitor of kappaB (IκB) protein and subsequent nuclear translocation of p65. As a result, chrysin suppressed the expression of NF-κB-targeted anti-apoptotic gene, c-FLIP-L. The role of c-FLIP-L was further confirmed by its ectopic expression, which significantly Protected Cell death induced by combined treatment with chrysin and TNFα. Data from this study thus reveal a novel function of chrysin and enhance the value of chrysin as an anti-cancer agent.
Ranxi Shi - One of the best experts on this subject based on the ideXlab platform.
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luteolin sensitizes tumor necrosis factor α induced apoptosis in human tumor Cells
Oncogene, 2004Co-Authors: Ranxi Shi, Choon Nam Ong, Hanming SheAbstract:Tumor necrosis factor-α (TNFα) activates both Cell death and Cell survival pathways, which render most cancer Cells resistant to its cytotoxicity. In this study, we found that pretreatment with luteolin, a plant flavonoid, greatly sensitized TNFα-induced apoptotic Cell death in a number of human cancer Cell lines; including colorectal cancer COLO205, HCT116 Cells and cervical cancer HeLa Cells. In the search of the molecular mechanisms responsible for the sensitization effect of luteolin, we discovered that luteolin inhibited TNFα-induced activation of nuclear transcription factor-kappa B (NF-κB), the main survival factor in TNFα signaling. As a result, luteolin suppressed the expression of NF-κB-targeted antiapoptotic genes, including A20 and Cellular inhibitor of apoptosis protein-1 (c-IAP1). The role of A20 and c-IAP1 was further confirmed by ectopic expression of these two genes, which significantly Protected Cell death induced by luteolin followed by TNFα. In addition, inhibition of NF-κB by luteolin led to augmentation and prolongation of c-Jun N-terminal kinase (JNK) activation induced by TNFα. Suppression of JNK activation, either by a synthetic JNK inhibitor (SP600125) or by overexpression of the dominant negative forms of JNK kinase 1 (JNKK1) and JNK kinase 2 (JNKK2), conferred significant protection against apoptotic Cell death induced by luteolin and TNFα, suggesting that NF-κB and JNK are closely associated with the sensitization effect of luteolin. Data from this study reveal a novel function of luteolin and enhance the value of luteolin as an anticancer agent.
Xingfen Yang - One of the best experts on this subject based on the ideXlab platform.
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chrysin sensitizes tumor necrosis factor α induced apoptosis in human tumor Cells via suppression of nuclear factor kappab
Cancer Letters, 2010Co-Authors: Xin Li, Qing Huang, Xingfen Yang, Hanming ShenAbstract:Abstract Chrysin (5,7-dihydroxyflavone) is a natural flavonoid commonly found in many plants. The anti-cancer property of chrysin has been demonstrated although the molecular mechanisms remain to be further elucidated. In the present study, we found that, pretreatment with chrysin greatly sensitized various human cancer Cells to tumor necrosis factor-alpha (TNFα)-induced apoptosis. In the search of the molecular mechanisms responsible for the sensitization effect of chrysin, we discovered that such sensitization is closely associated with the inhibitory effect of chrysin on TNFα-mediated nuclear transcription factor-kappaB (NF-κB) activation. Pretreatment with chrysin inhibited TNFα-induced degradation of Inhibitor of kappaB (IκB) protein and subsequent nuclear translocation of p65. As a result, chrysin suppressed the expression of NF-κB-targeted anti-apoptotic gene, c-FLIP-L. The role of c-FLIP-L was further confirmed by its ectopic expression, which significantly Protected Cell death induced by combined treatment with chrysin and TNFα. Data from this study thus reveal a novel function of chrysin and enhance the value of chrysin as an anti-cancer agent.
