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Chung Soo Lee - One of the best experts on this subject based on the ideXlab platform.
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Combined effect of protein kinase B inhibitor or extracellular signal-regulated kinase inhibitor against farnesyltransferase inhibition-induced apoptosis in SiHa cells
Naunyn-Schmiedeberg's Archives of Pharmacology, 2008Co-Authors: Sun Joo Lee, Chung Soo LeeAbstract:The present study investigated the combined effect of Akt or extracellular signal-regulated kinase (ERK) inhibition in the presence of farnesyltransferase inhibitor against human cervix and Uterus Tumor cell line SiHa cells. Farnesyltransferase inhibitor may induce apoptosis through the mitochondria-mediated process and inhibition of the MEK, ERK, and Akt activity. Inhibitors of Akt and ERK at low concentrations seem to prevent the farnesyltransferase inhibitor-induced apoptosis in cervical SiHa cells by suppressing the mitochondrial membrane permeability change that leads to cytochrome c release and caspase-3 activation. These effects may be associated with inhibition of the reactive oxygen species formation and glutathione depletion. In contrast, at higher concentrations more than 1 μM, the Akt inhibitor and ERK inhibitor seem to exhibit an additive toxic effect against farnesyltransferase inhibitor-induced apoptosis by increasing mitochondrial membrane permeability change and oxidative stress, which may not involve inhibition of MEK, ERK, and Akt activity.
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18β-Glycyrrhetinic acid induces apoptotic cell death in SiHa cells and exhibits a synergistic effect against antibiotic anti-cancer drug toxicity
Life Sciences, 2008Co-Authors: Chung Soo Lee, Yun Jeong Kim, Min Sung Lee, Eun Sook Han, Sun Joo LeeAbstract:Abstract Defects in mitochondrial function have been shown to participate in the induction of cell death in cancer cells. The present study was designed to assess the toxic effect of 18β-glycyrrhetinic acid against human cervix and Uterus Tumor cell line SiHa cells in relation to the mitochondria-mediated cell-death process and evaluate the combined toxic effect of 18β-glycyrrhetinic acid and anti-cancer drugs. 18β-Glycyrrhetinic acid induced the nuclear damage, changes in the mitochondrial membrane permeability, formation of reactive oxygen species and depletion of glutathione in SiHa cells. It caused cell death by inducing the increase in the pro-apoptotic Bax protein and cytochrome c levels, reduction in anti-apoptotic Bcl-2 level, subsequent caspase-3 activation and loss of the mitochondrial transmembrane potential. Unlike 18β-glycyrrhetinic acid, a pro-compound glycyrrhizin up to 100 µM did not induce cell death and depletion of glutathione. Combined treatment of mitomycin c (or doxorubicin) and 18β-glycyrrhetinic acid revealed a synergistic toxic effect. Meanwhile, combination of camptothecin and 18β-glycyrrhetinic acid exhibited an additive cytotoxic effect. Results suggest that 18β-glycyrrhetinic acid may cause cell death in SiHa cells by inducing the mitochondrial membrane permeability change, leading to cytochrome c release and caspase-3 activation. The effect may be associated with increased formation of reactive oxygen species and depletion of glutathione. Combined treatment of antibiotic anti-cancer drug and 18β-glycyrrhetinic acid seems to exhibit a synergistic toxic effect.
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18beta-Glycyrrhetinic acid induces apoptotic cell death in SiHa cells and exhibits a synergistic effect against antibiotic anti-cancer drug toxicity.
Life Sciences, 2008Co-Authors: Chung Soo Lee, Yun Jeong Kim, Min Sung Lee, Eun Sook Han, Sun Joo LeeAbstract:Defects in mitochondrial function have been shown to participate in the induction of cell death in cancer cells. The present study was designed to assess the toxic effect of 18beta-glycyrrhetinic acid against human cervix and Uterus Tumor cell line SiHa cells in relation to the mitochondria-mediated cell-death process and evaluate the combined toxic effect of 18beta-glycyrrhetinic acid and anti-cancer drugs. 18beta-Glycyrrhetinic acid induced the nuclear damage, changes in the mitochondrial membrane permeability, formation of reactive oxygen species and depletion of glutathione in SiHa cells. It caused cell death by inducing the increase in the pro-apoptotic Bax protein and cytochrome c levels, reduction in anti-apoptotic Bcl-2 level, subsequent caspase-3 activation and loss of the mitochondrial transmembrane potential. Unlike 18beta-glycyrrhetinic acid, a pro-compound glycyrrhizin up to 100 microM did not induce cell death and depletion of glutathione. Combined treatment of mitomycin c (or doxorubicin) and 18beta-glycyrrhetinic acid revealed a synergistic toxic effect. Meanwhile, combination of camptothecin and 18beta-glycyrrhetinic acid exhibited an additive cytotoxic effect. Results suggest that 18beta-glycyrrhetinic acid may cause cell death in SiHa cells by inducing the mitochondrial membrane permeability change, leading to cytochrome c release and caspase-3 activation. The effect may be associated with increased formation of reactive oxygen species and depletion of glutathione. Combined treatment of antibiotic anti-cancer drug and 18beta-glycyrrhetinic acid seems to exhibit a synergistic toxic effect.
Gui-yuan Li - One of the best experts on this subject based on the ideXlab platform.
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In silico expression analysis of human novel gene UBAP1 in multiple cancers
Chinese Journal of Cancer Research, 2002Co-Authors: Jun Qina, Ke Tang, Wei-fang Li, Rong Wang, Gui-yuan LiAbstract:Objective: To identify the differential expression profile of human novel gene UBAP1, a putative nasopharyngeal neoplasms (NPC) relate gene, in multiple cancers. Methods: We first present an EST approach for electronic Northern in silico to analyse expression patterns of UBAP1 in Tumor and normal tissues. Full length cDNA of UBAP1 gene was taken as a “probe” sequence, and a blastn search was performed against human EST Database. The Blastn report can be used to determine the fold differences between the pedigree ESTs in different libraries. Especially, the ESTs corresponding to UBAP1 present in fifteen Tumor-derived libraries were compared against their normal counterpart to produce an electronic differential expression profile. Second, the distinct down-regulation of UBAP1 in meningioma, glioma, and colorectal Tumor was confirmed by differentially RT-PCR analysis. Results: Database surveys indicated that UBAP1 gene was not only ubiquitously expressed in many normal tissues with various levels but also differentially expressed in different Tumor tissues, especially down-regulated in multiple neoplastic tissues such as brain, breast, skin, colon, testis and Uterus Tumor tissues. Furthermore, differential RT-PCR analysis demonstrated that expression of UBAP1 was down-regulated or absent in 7 of 12 (58%) meningioma samples, 6 of 9 (66%) glioma and 7 of 11 (63%) colorectal Tumor tissues respectively. Conclusion: we described a data mining procedure in silico that proved to be useful for the identification of differential expression patterns of UBAP1. These findings could be valuable for the investigation of the mechanism the differential expression of UBAP1 gene and its significance in the progression of multiple cancers.
Sun Joo Lee - One of the best experts on this subject based on the ideXlab platform.
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Combined effect of protein kinase B inhibitor or extracellular signal-regulated kinase inhibitor against farnesyltransferase inhibition-induced apoptosis in SiHa cells
Naunyn-Schmiedeberg's Archives of Pharmacology, 2008Co-Authors: Sun Joo Lee, Chung Soo LeeAbstract:The present study investigated the combined effect of Akt or extracellular signal-regulated kinase (ERK) inhibition in the presence of farnesyltransferase inhibitor against human cervix and Uterus Tumor cell line SiHa cells. Farnesyltransferase inhibitor may induce apoptosis through the mitochondria-mediated process and inhibition of the MEK, ERK, and Akt activity. Inhibitors of Akt and ERK at low concentrations seem to prevent the farnesyltransferase inhibitor-induced apoptosis in cervical SiHa cells by suppressing the mitochondrial membrane permeability change that leads to cytochrome c release and caspase-3 activation. These effects may be associated with inhibition of the reactive oxygen species formation and glutathione depletion. In contrast, at higher concentrations more than 1 μM, the Akt inhibitor and ERK inhibitor seem to exhibit an additive toxic effect against farnesyltransferase inhibitor-induced apoptosis by increasing mitochondrial membrane permeability change and oxidative stress, which may not involve inhibition of MEK, ERK, and Akt activity.
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18β-Glycyrrhetinic acid induces apoptotic cell death in SiHa cells and exhibits a synergistic effect against antibiotic anti-cancer drug toxicity
Life Sciences, 2008Co-Authors: Chung Soo Lee, Yun Jeong Kim, Min Sung Lee, Eun Sook Han, Sun Joo LeeAbstract:Abstract Defects in mitochondrial function have been shown to participate in the induction of cell death in cancer cells. The present study was designed to assess the toxic effect of 18β-glycyrrhetinic acid against human cervix and Uterus Tumor cell line SiHa cells in relation to the mitochondria-mediated cell-death process and evaluate the combined toxic effect of 18β-glycyrrhetinic acid and anti-cancer drugs. 18β-Glycyrrhetinic acid induced the nuclear damage, changes in the mitochondrial membrane permeability, formation of reactive oxygen species and depletion of glutathione in SiHa cells. It caused cell death by inducing the increase in the pro-apoptotic Bax protein and cytochrome c levels, reduction in anti-apoptotic Bcl-2 level, subsequent caspase-3 activation and loss of the mitochondrial transmembrane potential. Unlike 18β-glycyrrhetinic acid, a pro-compound glycyrrhizin up to 100 µM did not induce cell death and depletion of glutathione. Combined treatment of mitomycin c (or doxorubicin) and 18β-glycyrrhetinic acid revealed a synergistic toxic effect. Meanwhile, combination of camptothecin and 18β-glycyrrhetinic acid exhibited an additive cytotoxic effect. Results suggest that 18β-glycyrrhetinic acid may cause cell death in SiHa cells by inducing the mitochondrial membrane permeability change, leading to cytochrome c release and caspase-3 activation. The effect may be associated with increased formation of reactive oxygen species and depletion of glutathione. Combined treatment of antibiotic anti-cancer drug and 18β-glycyrrhetinic acid seems to exhibit a synergistic toxic effect.
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18beta-Glycyrrhetinic acid induces apoptotic cell death in SiHa cells and exhibits a synergistic effect against antibiotic anti-cancer drug toxicity.
Life Sciences, 2008Co-Authors: Chung Soo Lee, Yun Jeong Kim, Min Sung Lee, Eun Sook Han, Sun Joo LeeAbstract:Defects in mitochondrial function have been shown to participate in the induction of cell death in cancer cells. The present study was designed to assess the toxic effect of 18beta-glycyrrhetinic acid against human cervix and Uterus Tumor cell line SiHa cells in relation to the mitochondria-mediated cell-death process and evaluate the combined toxic effect of 18beta-glycyrrhetinic acid and anti-cancer drugs. 18beta-Glycyrrhetinic acid induced the nuclear damage, changes in the mitochondrial membrane permeability, formation of reactive oxygen species and depletion of glutathione in SiHa cells. It caused cell death by inducing the increase in the pro-apoptotic Bax protein and cytochrome c levels, reduction in anti-apoptotic Bcl-2 level, subsequent caspase-3 activation and loss of the mitochondrial transmembrane potential. Unlike 18beta-glycyrrhetinic acid, a pro-compound glycyrrhizin up to 100 microM did not induce cell death and depletion of glutathione. Combined treatment of mitomycin c (or doxorubicin) and 18beta-glycyrrhetinic acid revealed a synergistic toxic effect. Meanwhile, combination of camptothecin and 18beta-glycyrrhetinic acid exhibited an additive cytotoxic effect. Results suggest that 18beta-glycyrrhetinic acid may cause cell death in SiHa cells by inducing the mitochondrial membrane permeability change, leading to cytochrome c release and caspase-3 activation. The effect may be associated with increased formation of reactive oxygen species and depletion of glutathione. Combined treatment of antibiotic anti-cancer drug and 18beta-glycyrrhetinic acid seems to exhibit a synergistic toxic effect.
Hitomi Nakamura - One of the best experts on this subject based on the ideXlab platform.
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ORIGINAL ARTICLE: Temporal and Spatial Expression of Tumor-Associated Antigen RCAS1 in Pregnant Mouse Uterus: Tumor-ASSOCIATED PROTEIN RCAS1 IN PREGNANT MICE
American Journal of Reproductive Immunology, 2009Co-Authors: Ekaterine Tskitishvili, Hitomi Nakamura, Yukiko Kinugasa-taniguchi, Takeshi Kanagawa, Tadashi Kimura, Takuji Tomimatsu, Koichiro ShimoyaAbstract:PROBLEM The Tumor-associated antigen RCAS1 (receptor-binding cancer antigen expressed on SiSo cells) is considered to play a role in the inhibition of maternal immune response during pregnancy, and participates in the initiation of labor and placental detachment. The aim of our study was to investigate the expression of RCAS1 protein in the uteri of normal pregnant mice. METHOD of study Uteri with fetuses were collected from pregnant ICR mice on days 1.5, 3.5, 5.5, 7.5, and 9.5 p.c., and uterine and placental tissues were obtained separately on days 11.5, 13.5, 15.5, and 17.5 p.c. Samples were examined using real-time (RT)-PCR, Western blotting, and immunohistochemical analyses. RESULTS In normal pregnant mice, RCAS1 protein mRNA was significantly increased on day 7.5 p.c. Antigen localization was detected in the placenta, decidua, and fetus. CONCLUSION The results of this study suggest the importance of day 7.5 p.c. for RCAS1 protein expression in connection with placentation as a possible target for future in vivo studies.
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hemagglutinating virus of japan hvj envelope vector as a versatile gene delivery system
Molecular Therapy, 2002Co-Authors: Yasufumi Kaneda, Tomoyuki Nishikawa, Hiroyuki Ikegami, Naho Suzuki, Ryuichi Morishita, Toshihiro Nakajima, Hitomi Nakamura, Seiji Yamamoto, Hitoshi KotaniAbstract:We have developed a simple method for converting the lipid envelope of an inactivated virus to a gene transfer vector. Hemagglutinating virus of Japan (HVJ; Sendai virus) envelope vector was constructed by incorporating plasmid DNA into inactivated HVJ particles. This HVJ envelope vector introduced plasmid DNA efficiently and rapidly into various cell lines, including cancer cells and several types of primary cell culture. Efficiency of gene transfer was greatly enhanced by protamine sulfate and centrifugation. Fluorescein isothiocyanate-labeled oligodeoxynucleotides (FITC-ODN) were also delivered to cells at > 95% efficiency. When HVJ envelope vector was injected into organs directly, reporter gene expression was observed in organs including liver, brain, skin, Uterus, Tumor masses, lung, and eye. When HVJ envelope vector containing luciferase gene was injected into mouse tail vein, luciferase gene expression was detected primarily in spleen. FITC-ODN were also delivered to spleen cells by intravenous injection of HVJ envelope. These results suggest that HVJ envelope vector will be useful for both ex vivo and in vivo gene therapy experiments.
Rong Wang - One of the best experts on this subject based on the ideXlab platform.
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In silico expression analysis of human novel gene UBAP1 in multiple cancers
Chinese Journal of Cancer Research, 2002Co-Authors: Jun Qina, Ke Tang, Wei-fang Li, Rong Wang, Gui-yuan LiAbstract:Objective: To identify the differential expression profile of human novel gene UBAP1, a putative nasopharyngeal neoplasms (NPC) relate gene, in multiple cancers. Methods: We first present an EST approach for electronic Northern in silico to analyse expression patterns of UBAP1 in Tumor and normal tissues. Full length cDNA of UBAP1 gene was taken as a “probe” sequence, and a blastn search was performed against human EST Database. The Blastn report can be used to determine the fold differences between the pedigree ESTs in different libraries. Especially, the ESTs corresponding to UBAP1 present in fifteen Tumor-derived libraries were compared against their normal counterpart to produce an electronic differential expression profile. Second, the distinct down-regulation of UBAP1 in meningioma, glioma, and colorectal Tumor was confirmed by differentially RT-PCR analysis. Results: Database surveys indicated that UBAP1 gene was not only ubiquitously expressed in many normal tissues with various levels but also differentially expressed in different Tumor tissues, especially down-regulated in multiple neoplastic tissues such as brain, breast, skin, colon, testis and Uterus Tumor tissues. Furthermore, differential RT-PCR analysis demonstrated that expression of UBAP1 was down-regulated or absent in 7 of 12 (58%) meningioma samples, 6 of 9 (66%) glioma and 7 of 11 (63%) colorectal Tumor tissues respectively. Conclusion: we described a data mining procedure in silico that proved to be useful for the identification of differential expression patterns of UBAP1. These findings could be valuable for the investigation of the mechanism the differential expression of UBAP1 gene and its significance in the progression of multiple cancers.
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Identification of digital differential expression patterns of a novel human gene (UBAP1) by an expressed sequence tag strategy
Ai zheng = Aizheng = Chinese journal of cancer, 2002Co-Authors: Jun Qian, Xi Zhang, Wang, Rong WangAbstract:BACKGROUND & OBJECTIVES This study was designed to identify differential expression patterns in Tumor and normal tissues of the human novel gene, UBAP1, a putative nasopharyngeal carcinoma (NPC) relate gene, which is located at human chromosome 9p21-22 where loss of heterozygosity frequently occurs in NPC. METHODS Based on the generation of expressed sequence tags (ESTs), in the authors' electronic Northern blot, complete cDNA of ubap1 gene was taken as a "probe" sequence, and human EST Database search of GenBank was carried out using BLASTn programs. A report generated in a BLAST search of ubap1 gene sequence against an EST database consisting of such 'pedigree' ESTs allows the inference of the gene's tissue distribution. Furthermore, differential RT-PCR was used to describe the expression patterns of ubap1 in partial Tumor tissues. RESULTS Database surveys indicated ubap1 gene was not only ubiquitously expressed in many normal tissues with various levels but also differentially expressed in different Tumor tissues, especially down-regulated in multiple neoplastic tissues such as brain, breast, skin, colon, testis, and Uterus Tumor tissues. Furthermore, differential RT-PCR analysis demonstrated expression of ubap1 was down-regulated or absent in 7 of 11(64%) meningioma samples and 13 of 18 (72%) colorectal Tumor tissues respectively. CONCLUSIONS The authors present an EST approach that proved to be useful for the identification of differential expression patterns of ubap1 in different Tumors. These findings could be valuable for the investigation of the mechanism of UBAP1 gene exhibiting differential expression, potentially involved in the progression of multiple cancers.
