The Experts below are selected from a list of 318 Experts worldwide ranked by ideXlab platform
Sung-kwon Moon - One of the best experts on this subject based on the ideXlab platform.
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Esculetin inhibits Cell proliferation through the Ras/ERK1/2 pathway in human colon cancer Cells.
Oncology reports, 2011Co-Authors: Sung-suk Park, Jung-hyurk Lim, Wun-jae Kim, Sung Kyu Park, Yung Hyun Choi, Sung-kwon MoonAbstract:Esculetin, a phenolic compound, has been shown to inhibit the growth of colon tumors in animal studies. However, the roles of signaling pathways and Cell cycle regulation in the esculetin-induced inhibition of cancer Cell growth, remain to be elucidated. The present study suggests a novel mechanism for the Ras/ERK1/2 pathway in esculetin-treated human colon cancer HCT116 Cells. The treatment of Cells with esculetin resulted in significant growth inhibition and G1 Phase Cell cycle arrest, which led to the down-regulation of cyclin and cyclin-dependent kinase (CDK) expressions. This G1 Phase Cell cycle arrest was associated with the up-regulation of p27KIP expression. In addition, ERK1/2 was activated by esculetin. The pre-treatment of Cells with the MEK1/2-specific inhibitor, PD98059, blocked the p27KIP expression induced by esculetin. Blockage of the ERK1/2 function consistently prevented the inhibition of Cell proliferation and decreased G1 Phase Cell cycle protein levels. Furthermore, Ras activation was increased by the esculetin treatment. Transient transfection of the dominant negative Ras (RasN17) mutant gene abolished both the ERK1/2 activity and p27KIP expression induced by esculetin. Finally, the overexpression of RasN17 suppressed the esculetin-induced reduction in Cell proliferation and Cell cycle proteins. In conclusion, these results indicate that the Ras/ERK1/2 pathway is mediated by the p27KIP1 induction, leading to a reduction in cyclin/CDK complexes in the esculetin-induced inhibition of colon cancer Cell growth. Overall, these findings indicate that the molecular action of esculetin has therapeutic potential for the treatment of colon malignancies.
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esculetin inhibits Cell proliferation through the ras erk1 2 pathway in human colon cancer Cells
Oncology Reports, 2010Co-Authors: Sung-suk Park, Jung-hyurk Lim, Wun-jae Kim, Sung Kyu Park, Yung Hyun Choi, Sung-kwon MoonAbstract:Esculetin, a phenolic compound, has been shown to inhibit the growth of colon tumors in animal studies. However, the roles of signaling pathways and Cell cycle regulation in the esculetin-induced inhibition of cancer Cell growth, remain to be elucidated. The present study suggests a novel mechanism for the Ras/ERK1/2 pathway in esculetin-treated human colon cancer HCT116 Cells. The treatment of Cells with esculetin resulted in significant growth inhibition and G1 Phase Cell cycle arrest, which led to the down-regulation of cyclin and cyclin-dependent kinase (CDK) expressions. This G1 Phase Cell cycle arrest was associated with the up-regulation of p27KIP expression. In addition, ERK1/2 was activated by esculetin. The pre-treatment of Cells with the MEK1/2-specific inhibitor, PD98059, blocked the p27KIP expression induced by esculetin. Blockage of the ERK1/2 function consistently prevented the inhibition of Cell proliferation and decreased G1 Phase Cell cycle protein levels. Furthermore, Ras activation was increased by the esculetin treatment. Transient transfection of the dominant negative Ras (RasN17) mutant gene abolished both the ERK1/2 activity and p27KIP expression induced by esculetin. Finally, the overexpression of RasN17 suppressed the esculetin-induced reduction in Cell proliferation and Cell cycle proteins. In conclusion, these results indicate that the Ras/ERK1/2 pathway is mediated by the p27KIP1 induction, leading to a reduction in cyclin/CDK complexes in the esculetin-induced inhibition of colon cancer Cell growth. Overall, these findings indicate that the molecular action of esculetin has therapeutic potential for the treatment of colon malignancies.
Haibo Pan - One of the best experts on this subject based on the ideXlab platform.
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synergistic effect of black tea polyphenol theaflavin 3 3 digallate with cisplatin against cisplatin resistant human ovarian cancer Cells
Journal of Functional Foods, 2018Co-Authors: Haibo Pan, Gary O Rankin, Yon Rojanasakul, Yi Charlie ChenAbstract:Theaflavin-3, 3'-digallate (TF3) is a phenolic compound extracted from black tea. We previously demonstrated that TF3 selectively inhibited ovarian cancer Cells. Ovarian cancer has high death rate because of acquired cisplatin resistance. We aimed to investigate the synergistic effect of TF3 and cisplatin (CDDP) against cisplatin resistant ovarian cancer Cells. In the present study, combination treatment with TF3 and CDDP showed a synergistic cytotoxic effect in A2780/CP70 and OVCAR3 Cells. Combination treatment showed a synergistic pro-apoptotic effect and synergistically induced G1/S Phase Cell cycle arrest. Synergistic apoptosis was accompanied by regulating protein expression of cleaved caspase 3/7, cytochrome c, Bax and Bcl-2. Combination treatment induced G1/S Phase Cell cycle arrest via regulating protein expression of cyclin A2, cyclin D1, cyclin E1 and CDK2/4. Combination treatment could synergistically down-regulate Akt phosphorylation in both Cell lines. TF3 may be used as an adjuvant for the treatment of advanced ovarian cancer.
Yi Charlie Chen - One of the best experts on this subject based on the ideXlab platform.
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synergistic effect of black tea polyphenol theaflavin 3 3 digallate with cisplatin against cisplatin resistant human ovarian cancer Cells
Journal of Functional Foods, 2018Co-Authors: Haibo Pan, Gary O Rankin, Yon Rojanasakul, Yi Charlie ChenAbstract:Theaflavin-3, 3'-digallate (TF3) is a phenolic compound extracted from black tea. We previously demonstrated that TF3 selectively inhibited ovarian cancer Cells. Ovarian cancer has high death rate because of acquired cisplatin resistance. We aimed to investigate the synergistic effect of TF3 and cisplatin (CDDP) against cisplatin resistant ovarian cancer Cells. In the present study, combination treatment with TF3 and CDDP showed a synergistic cytotoxic effect in A2780/CP70 and OVCAR3 Cells. Combination treatment showed a synergistic pro-apoptotic effect and synergistically induced G1/S Phase Cell cycle arrest. Synergistic apoptosis was accompanied by regulating protein expression of cleaved caspase 3/7, cytochrome c, Bax and Bcl-2. Combination treatment induced G1/S Phase Cell cycle arrest via regulating protein expression of cyclin A2, cyclin D1, cyclin E1 and CDK2/4. Combination treatment could synergistically down-regulate Akt phosphorylation in both Cell lines. TF3 may be used as an adjuvant for the treatment of advanced ovarian cancer.
Sung-suk Park - One of the best experts on this subject based on the ideXlab platform.
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Esculetin inhibits Cell proliferation through the Ras/ERK1/2 pathway in human colon cancer Cells.
Oncology reports, 2011Co-Authors: Sung-suk Park, Jung-hyurk Lim, Wun-jae Kim, Sung Kyu Park, Yung Hyun Choi, Sung-kwon MoonAbstract:Esculetin, a phenolic compound, has been shown to inhibit the growth of colon tumors in animal studies. However, the roles of signaling pathways and Cell cycle regulation in the esculetin-induced inhibition of cancer Cell growth, remain to be elucidated. The present study suggests a novel mechanism for the Ras/ERK1/2 pathway in esculetin-treated human colon cancer HCT116 Cells. The treatment of Cells with esculetin resulted in significant growth inhibition and G1 Phase Cell cycle arrest, which led to the down-regulation of cyclin and cyclin-dependent kinase (CDK) expressions. This G1 Phase Cell cycle arrest was associated with the up-regulation of p27KIP expression. In addition, ERK1/2 was activated by esculetin. The pre-treatment of Cells with the MEK1/2-specific inhibitor, PD98059, blocked the p27KIP expression induced by esculetin. Blockage of the ERK1/2 function consistently prevented the inhibition of Cell proliferation and decreased G1 Phase Cell cycle protein levels. Furthermore, Ras activation was increased by the esculetin treatment. Transient transfection of the dominant negative Ras (RasN17) mutant gene abolished both the ERK1/2 activity and p27KIP expression induced by esculetin. Finally, the overexpression of RasN17 suppressed the esculetin-induced reduction in Cell proliferation and Cell cycle proteins. In conclusion, these results indicate that the Ras/ERK1/2 pathway is mediated by the p27KIP1 induction, leading to a reduction in cyclin/CDK complexes in the esculetin-induced inhibition of colon cancer Cell growth. Overall, these findings indicate that the molecular action of esculetin has therapeutic potential for the treatment of colon malignancies.
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esculetin inhibits Cell proliferation through the ras erk1 2 pathway in human colon cancer Cells
Oncology Reports, 2010Co-Authors: Sung-suk Park, Jung-hyurk Lim, Wun-jae Kim, Sung Kyu Park, Yung Hyun Choi, Sung-kwon MoonAbstract:Esculetin, a phenolic compound, has been shown to inhibit the growth of colon tumors in animal studies. However, the roles of signaling pathways and Cell cycle regulation in the esculetin-induced inhibition of cancer Cell growth, remain to be elucidated. The present study suggests a novel mechanism for the Ras/ERK1/2 pathway in esculetin-treated human colon cancer HCT116 Cells. The treatment of Cells with esculetin resulted in significant growth inhibition and G1 Phase Cell cycle arrest, which led to the down-regulation of cyclin and cyclin-dependent kinase (CDK) expressions. This G1 Phase Cell cycle arrest was associated with the up-regulation of p27KIP expression. In addition, ERK1/2 was activated by esculetin. The pre-treatment of Cells with the MEK1/2-specific inhibitor, PD98059, blocked the p27KIP expression induced by esculetin. Blockage of the ERK1/2 function consistently prevented the inhibition of Cell proliferation and decreased G1 Phase Cell cycle protein levels. Furthermore, Ras activation was increased by the esculetin treatment. Transient transfection of the dominant negative Ras (RasN17) mutant gene abolished both the ERK1/2 activity and p27KIP expression induced by esculetin. Finally, the overexpression of RasN17 suppressed the esculetin-induced reduction in Cell proliferation and Cell cycle proteins. In conclusion, these results indicate that the Ras/ERK1/2 pathway is mediated by the p27KIP1 induction, leading to a reduction in cyclin/CDK complexes in the esculetin-induced inhibition of colon cancer Cell growth. Overall, these findings indicate that the molecular action of esculetin has therapeutic potential for the treatment of colon malignancies.
Yung Hyun Choi - One of the best experts on this subject based on the ideXlab platform.
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Esculetin inhibits Cell proliferation through the Ras/ERK1/2 pathway in human colon cancer Cells.
Oncology reports, 2011Co-Authors: Sung-suk Park, Jung-hyurk Lim, Wun-jae Kim, Sung Kyu Park, Yung Hyun Choi, Sung-kwon MoonAbstract:Esculetin, a phenolic compound, has been shown to inhibit the growth of colon tumors in animal studies. However, the roles of signaling pathways and Cell cycle regulation in the esculetin-induced inhibition of cancer Cell growth, remain to be elucidated. The present study suggests a novel mechanism for the Ras/ERK1/2 pathway in esculetin-treated human colon cancer HCT116 Cells. The treatment of Cells with esculetin resulted in significant growth inhibition and G1 Phase Cell cycle arrest, which led to the down-regulation of cyclin and cyclin-dependent kinase (CDK) expressions. This G1 Phase Cell cycle arrest was associated with the up-regulation of p27KIP expression. In addition, ERK1/2 was activated by esculetin. The pre-treatment of Cells with the MEK1/2-specific inhibitor, PD98059, blocked the p27KIP expression induced by esculetin. Blockage of the ERK1/2 function consistently prevented the inhibition of Cell proliferation and decreased G1 Phase Cell cycle protein levels. Furthermore, Ras activation was increased by the esculetin treatment. Transient transfection of the dominant negative Ras (RasN17) mutant gene abolished both the ERK1/2 activity and p27KIP expression induced by esculetin. Finally, the overexpression of RasN17 suppressed the esculetin-induced reduction in Cell proliferation and Cell cycle proteins. In conclusion, these results indicate that the Ras/ERK1/2 pathway is mediated by the p27KIP1 induction, leading to a reduction in cyclin/CDK complexes in the esculetin-induced inhibition of colon cancer Cell growth. Overall, these findings indicate that the molecular action of esculetin has therapeutic potential for the treatment of colon malignancies.
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esculetin inhibits Cell proliferation through the ras erk1 2 pathway in human colon cancer Cells
Oncology Reports, 2010Co-Authors: Sung-suk Park, Jung-hyurk Lim, Wun-jae Kim, Sung Kyu Park, Yung Hyun Choi, Sung-kwon MoonAbstract:Esculetin, a phenolic compound, has been shown to inhibit the growth of colon tumors in animal studies. However, the roles of signaling pathways and Cell cycle regulation in the esculetin-induced inhibition of cancer Cell growth, remain to be elucidated. The present study suggests a novel mechanism for the Ras/ERK1/2 pathway in esculetin-treated human colon cancer HCT116 Cells. The treatment of Cells with esculetin resulted in significant growth inhibition and G1 Phase Cell cycle arrest, which led to the down-regulation of cyclin and cyclin-dependent kinase (CDK) expressions. This G1 Phase Cell cycle arrest was associated with the up-regulation of p27KIP expression. In addition, ERK1/2 was activated by esculetin. The pre-treatment of Cells with the MEK1/2-specific inhibitor, PD98059, blocked the p27KIP expression induced by esculetin. Blockage of the ERK1/2 function consistently prevented the inhibition of Cell proliferation and decreased G1 Phase Cell cycle protein levels. Furthermore, Ras activation was increased by the esculetin treatment. Transient transfection of the dominant negative Ras (RasN17) mutant gene abolished both the ERK1/2 activity and p27KIP expression induced by esculetin. Finally, the overexpression of RasN17 suppressed the esculetin-induced reduction in Cell proliferation and Cell cycle proteins. In conclusion, these results indicate that the Ras/ERK1/2 pathway is mediated by the p27KIP1 induction, leading to a reduction in cyclin/CDK complexes in the esculetin-induced inhibition of colon cancer Cell growth. Overall, these findings indicate that the molecular action of esculetin has therapeutic potential for the treatment of colon malignancies.
