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Josefa Leon - One of the best experts on this subject based on the ideXlab platform.
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inhibition of poly adenosine diphosphate ribose polymerase decreases hepatocellular carcinoma growth by modulation of tumor related Gene expression
Hepatology, 2010Co-Authors: Rosa Quilesperez, Jose Antonio Munozgamez, Angeles Ruizextremera, Francisco Ovalle, Laura Sanjuannunez, Ana Belen Martinalvarez, David Martinoliva, T Caballero, Paloma Rueda, Josefa LeonAbstract:Hepatocellular carcinoma (HCC) is associated with a poor prognosis due to a lack of effective treatment options. In HCC a significant role is played by DNA damage and the inflammatory response. Poly (ADP-ribose) polymerase-1 (PARP-1) is an important protein that regulates both these mechanisms. The objective of this study was to examine the effect of pharmacology PARP-1 inhibition on the reduction of tumor volume of HCC xenograft and on the hepatocarcinoGenesis induced by diethyl-nitrosamine (DEN). Pharmacologic PARP-1 inhibition with DPQ greatly reduces tumor xenograft volume with regard to a nontreated xenograft (394 mm3 versus 2,942 mm3, P < 0.05). This observation was paralleled by reductions in xenograft mitosis (P = 0.02) and tumor vasculoGenesis (P = 0.007, confirmed by in vitro angioGenesis study), as well as by an increase in the number of apoptotic cells in DPQ-treated mice (P = 0.04). A substantial difference in key Tumor-Related Gene expression (transformed 3T3 cell double minute 2 [MDM2], FLT1 [vascular endothelial growth factor receptor-1, VEGFR1], epidermal growth factor receptor [EPAS1]/hypoxia-inducible factor 2 [HIF2A], EGLN1 [PHD2], epidermal growth factor receptor [EGFR], MYC, JUND, SPP1 [OPN], hepatocyte growth factor [HGF]) was found between the control tumor xenografts and the PARP inhibitor-treated xenografts (data confirmed in HCC cell lines using PARP inhibitors and PARP-1 small interfering RNA [siRNA]). Furthermore, the results obtained in mice treated with DEN to induce hepatocarcinoGenesis showed, after treatment with a PARP inhibitor (DPQ), a significant reduction both in preneoplastic foci and in the expression of preneoplastic markers and proinflammatory Genes (Gstm3, Vegf, Spp1 [Opn], IL6, IL1b, and Tnf), bromodeoxyuridine incorporation, and NF-κB activation in the initial steps of carcinoGenesis (P < 0.05). Conclusion: This study shows that PARP inhibition is capable of controlling HCC growth and preventing tumor vasculoGenesis by regulating the activation of different Genes involved in tumor progression. (HEPATOLOGY 2010;51:255–266.)
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Inhibition of poly adenosine diphosphate‐ribose polymerase decreases hepatocellular carcinoma growth by modulation of tumor‐related Gene expression
Hepatology (Baltimore Md.), 2009Co-Authors: Rosa Quiles-pérez, T Caballero, Paloma Rueda, José Antonio Muñoz-gámez, Ángeles Ruiz-extremera, Francisco O'valle, Laura Sanjuan-nuñez, Ana Belén Martín‐Álvarez, David Martín-oliva, Josefa LeonAbstract:Hepatocellular carcinoma (HCC) is associated with a poor prognosis due to a lack of effective treatment options. In HCC a significant role is played by DNA damage and the inflammatory response. Poly (ADP-ribose) polymerase-1 (PARP-1) is an important protein that regulates both these mechanisms. The objective of this study was to examine the effect of pharmacology PARP-1 inhibition on the reduction of tumor volume of HCC xenograft and on the hepatocarcinoGenesis induced by diethyl-nitrosamine (DEN). Pharmacologic PARP-1 inhibition with DPQ greatly reduces tumor xenograft volume with regard to a nontreated xenograft (394 mm3 versus 2,942 mm3, P < 0.05). This observation was paralleled by reductions in xenograft mitosis (P = 0.02) and tumor vasculoGenesis (P = 0.007, confirmed by in vitro angioGenesis study), as well as by an increase in the number of apoptotic cells in DPQ-treated mice (P = 0.04). A substantial difference in key Tumor-Related Gene expression (transformed 3T3 cell double minute 2 [MDM2], FLT1 [vascular endothelial growth factor receptor-1, VEGFR1], epidermal growth factor receptor [EPAS1]/hypoxia-inducible factor 2 [HIF2A], EGLN1 [PHD2], epidermal growth factor receptor [EGFR], MYC, JUND, SPP1 [OPN], hepatocyte growth factor [HGF]) was found between the control tumor xenografts and the PARP inhibitor-treated xenografts (data confirmed in HCC cell lines using PARP inhibitors and PARP-1 small interfering RNA [siRNA]). Furthermore, the results obtained in mice treated with DEN to induce hepatocarcinoGenesis showed, after treatment with a PARP inhibitor (DPQ), a significant reduction both in preneoplastic foci and in the expression of preneoplastic markers and proinflammatory Genes (Gstm3, Vegf, Spp1 [Opn], IL6, IL1b, and Tnf), bromodeoxyuridine incorporation, and NF-κB activation in the initial steps of carcinoGenesis (P < 0.05). Conclusion: This study shows that PARP inhibition is capable of controlling HCC growth and preventing tumor vasculoGenesis by regulating the activation of different Genes involved in tumor progression. (HEPATOLOGY 2010;51:255–266.)
David Martín-oliva - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of poly adenosine diphosphate‐ribose polymerase decreases hepatocellular carcinoma growth by modulation of tumor‐related Gene expression
Hepatology (Baltimore Md.), 2009Co-Authors: Rosa Quiles-pérez, T Caballero, Paloma Rueda, José Antonio Muñoz-gámez, Ángeles Ruiz-extremera, Francisco O'valle, Laura Sanjuan-nuñez, Ana Belén Martín‐Álvarez, David Martín-oliva, Josefa LeonAbstract:Hepatocellular carcinoma (HCC) is associated with a poor prognosis due to a lack of effective treatment options. In HCC a significant role is played by DNA damage and the inflammatory response. Poly (ADP-ribose) polymerase-1 (PARP-1) is an important protein that regulates both these mechanisms. The objective of this study was to examine the effect of pharmacology PARP-1 inhibition on the reduction of tumor volume of HCC xenograft and on the hepatocarcinoGenesis induced by diethyl-nitrosamine (DEN). Pharmacologic PARP-1 inhibition with DPQ greatly reduces tumor xenograft volume with regard to a nontreated xenograft (394 mm3 versus 2,942 mm3, P < 0.05). This observation was paralleled by reductions in xenograft mitosis (P = 0.02) and tumor vasculoGenesis (P = 0.007, confirmed by in vitro angioGenesis study), as well as by an increase in the number of apoptotic cells in DPQ-treated mice (P = 0.04). A substantial difference in key Tumor-Related Gene expression (transformed 3T3 cell double minute 2 [MDM2], FLT1 [vascular endothelial growth factor receptor-1, VEGFR1], epidermal growth factor receptor [EPAS1]/hypoxia-inducible factor 2 [HIF2A], EGLN1 [PHD2], epidermal growth factor receptor [EGFR], MYC, JUND, SPP1 [OPN], hepatocyte growth factor [HGF]) was found between the control tumor xenografts and the PARP inhibitor-treated xenografts (data confirmed in HCC cell lines using PARP inhibitors and PARP-1 small interfering RNA [siRNA]). Furthermore, the results obtained in mice treated with DEN to induce hepatocarcinoGenesis showed, after treatment with a PARP inhibitor (DPQ), a significant reduction both in preneoplastic foci and in the expression of preneoplastic markers and proinflammatory Genes (Gstm3, Vegf, Spp1 [Opn], IL6, IL1b, and Tnf), bromodeoxyuridine incorporation, and NF-κB activation in the initial steps of carcinoGenesis (P < 0.05). Conclusion: This study shows that PARP inhibition is capable of controlling HCC growth and preventing tumor vasculoGenesis by regulating the activation of different Genes involved in tumor progression. (HEPATOLOGY 2010;51:255–266.)
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Inhibition of Poly(ADP-Ribose) Polymerase Modulates Tumor-Related Gene Expression, Including Hypoxia-Inducible Factor-1 Activation, during Skin CarcinoGenesis
Cancer research, 2006Co-Authors: David Martín-oliva, José Antonio Muñoz-gámez, Francisco O'valle, Rocío Aguilar-quesada, Rubén Martínez-romero, Raimundo G. Del Moral, José Mariano Ruiz De Almodóvar, Raquel Villuendas, Miguel A. Piris, F. Javier OliverAbstract:Poly(ADP-ribose) polymerase (PARP)-1, an enzyme that catalyzes the attachment of ADP ribose to target proteins, acts as a component of enhancer/promoter regulatory complexes. In the present study, we show that pharmacologic inhibition of PARP-1 with 3,4-dihydro-5-[4-(1-piperidinyl)butoxyl]-1(2H)isoquinolinone (DPQ) results in a strong delay in tumor formation and in a dramatic reduction in tumor size and multiplicity during 7,12-dimethylbenz(a)anthracene plus 12O-tetradecanoylphorbol-13-acetate–induced skin carcinoGenesis. This observation was parallel with a reduction in the skin inflammatory infiltrate in DPQ-treated mice and tumor vasculoGenesis. Inhibition of PARP also affected activator protein-1 (AP-1) activation but not nuclear factor-KB (NF-KB). Using cDNA expression array analysis, a substantial difference in key Tumor-Related Gene expression was found between chemically induced mice treated or not with PARP inhibitor and also between wild-type and parp-1 knockout mice. Most important differences were found in Gene expression for Nfkbiz, S100a9, Hif-1a, and other Genes involved in carcinoGenesis and inflammation. These results were corroborated by real-time PCR. Moreover, the transcriptional activity of hypoxia-inducible factor-1A (HIF-1A) was compromised by PARP inhibition or in PARP-1–deficient cells, as measured by Gene reporter assays and the expression of key target Genes for HIF-1A. Tumor vasculature was also strongly inhibited in PARP-1–deficient mice and by DPQ. In summary, this study shows that inhibition of PARP on itself is able to control tumor growth, and PARP inhibition or Genetic deletion of PARP-1 prevents from tumor promotion through their ability to cooperate with the activation AP-1, NF-KB, and HIF-1A. (Cancer Res 2006; 66(11): 5744-56)
Rosa Quilesperez - One of the best experts on this subject based on the ideXlab platform.
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inhibition of poly adenosine diphosphate ribose polymerase decreases hepatocellular carcinoma growth by modulation of tumor related Gene expression
Hepatology, 2010Co-Authors: Rosa Quilesperez, Jose Antonio Munozgamez, Angeles Ruizextremera, Francisco Ovalle, Laura Sanjuannunez, Ana Belen Martinalvarez, David Martinoliva, T Caballero, Paloma Rueda, Josefa LeonAbstract:Hepatocellular carcinoma (HCC) is associated with a poor prognosis due to a lack of effective treatment options. In HCC a significant role is played by DNA damage and the inflammatory response. Poly (ADP-ribose) polymerase-1 (PARP-1) is an important protein that regulates both these mechanisms. The objective of this study was to examine the effect of pharmacology PARP-1 inhibition on the reduction of tumor volume of HCC xenograft and on the hepatocarcinoGenesis induced by diethyl-nitrosamine (DEN). Pharmacologic PARP-1 inhibition with DPQ greatly reduces tumor xenograft volume with regard to a nontreated xenograft (394 mm3 versus 2,942 mm3, P < 0.05). This observation was paralleled by reductions in xenograft mitosis (P = 0.02) and tumor vasculoGenesis (P = 0.007, confirmed by in vitro angioGenesis study), as well as by an increase in the number of apoptotic cells in DPQ-treated mice (P = 0.04). A substantial difference in key Tumor-Related Gene expression (transformed 3T3 cell double minute 2 [MDM2], FLT1 [vascular endothelial growth factor receptor-1, VEGFR1], epidermal growth factor receptor [EPAS1]/hypoxia-inducible factor 2 [HIF2A], EGLN1 [PHD2], epidermal growth factor receptor [EGFR], MYC, JUND, SPP1 [OPN], hepatocyte growth factor [HGF]) was found between the control tumor xenografts and the PARP inhibitor-treated xenografts (data confirmed in HCC cell lines using PARP inhibitors and PARP-1 small interfering RNA [siRNA]). Furthermore, the results obtained in mice treated with DEN to induce hepatocarcinoGenesis showed, after treatment with a PARP inhibitor (DPQ), a significant reduction both in preneoplastic foci and in the expression of preneoplastic markers and proinflammatory Genes (Gstm3, Vegf, Spp1 [Opn], IL6, IL1b, and Tnf), bromodeoxyuridine incorporation, and NF-κB activation in the initial steps of carcinoGenesis (P < 0.05). Conclusion: This study shows that PARP inhibition is capable of controlling HCC growth and preventing tumor vasculoGenesis by regulating the activation of different Genes involved in tumor progression. (HEPATOLOGY 2010;51:255–266.)
Jie-ru Wang - One of the best experts on this subject based on the ideXlab platform.
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Expression of tumor related Gene NAG6 in gastric cancer and restriction fragment length polymorphism analysis.
World journal of gastroenterology, 2004Co-Authors: Xiao-mei Zhang, Shou-rong Sheng, Xiao-yan Wang, Liang-hua Bin, Jie-ru WangAbstract:AIM: NAG6 Gene is a novel tumor related Gene identified recently. This study was designed to examine the expression of this Gene in gastric cancer and corresponding normal tissues, and to investigate its role in the occurrence and development of gastric cancer, also to study if the Genetic structure of NAG6 was altered in gastric cancer. METHODS: Reverse transcription-polymerase chain reaction (RT-PCR), Northern blot analysis and dot hybridization were used to compare the expression level of NAG6 Gene in 42 cases of gastric cancer tissues with their corresponding normal tissues of the same patients respectively. In addition, restriction fragment length polymorphism (RFLP) analysis was adopted to study if the Genetic structure of NAG6 was altered in gastric carcinomas. RESULTS: The expression of NAG6 in 57.1% gastric cancer tissues (25/42) was absent by RT-PCR analysis. The down-regulation rate of NAG6 in gastric cancer tissues was significantly higher than that in corresponding normal tissues (P 0.05). Dot hybridization confirmed the results of RT-PCR. Furthermore, the results of EcoRI RFLP analysis of NAG6 Gene demonstrated that 3 of 7 cases of gastric cancer showed loss of 5 kb fragment in comparison with their corresponding normal tissues. CONCLUSION: NAG6 Gene is significantly down regulated in gastric cancer. The loss of Genetic materials may be the cause of down-regulation of NAG6 expression. This seems to suggest that NAG6 may represent a candidate of putative tumor suppressor Gene at 7q31-32 loci associated with gastric carcinoma. The down-regulation of this Gene may play a role in occurrence and development of this disease, however it may not be associated with lymph node and/or distance metastasis.
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Expression of tumor related Gene NGX6 in gastric cancer and colorectal cancer
2002Co-Authors: Xiao-mei Zhang, Shou-rong Sheng, Xiao-yan Wang, Jie-ru WangAbstract:Xiao-Mei Zhang, Xiao-Yan Wang, Department of Digistion Medicine,Xiangya Hospital, Central South University,Changsha 410008,HunanProvince,China.Shou-Rong Sheng, Department of Digistion Medicine,The thirdXiangya Hospital, Central South University,Changsha 410008,HunanProvince,China.Jie-Ru Wang, Jiang Li, Cancer Research Institute, School of XiangyaMedicine, Central South University, Changsha 410078, Hunan Province,China.Supported by the Nature Scientific Foundation of Hunan ProvinceNO.01JJY2102 and the National “863”project foundation of ChinaNo.102-10-01-05Correspondence to: Dr. Shou-Rong Sheng, Department of DigistionMedicine,The third Xiangya Hospital, Central South University,Changsha 410013,Hunan Province,China. tangyy@public.cs.hn.cnReceived 2002-04-01 Accepted 2002-05-22
Paloma Rueda - One of the best experts on this subject based on the ideXlab platform.
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inhibition of poly adenosine diphosphate ribose polymerase decreases hepatocellular carcinoma growth by modulation of tumor related Gene expression
Hepatology, 2010Co-Authors: Rosa Quilesperez, Jose Antonio Munozgamez, Angeles Ruizextremera, Francisco Ovalle, Laura Sanjuannunez, Ana Belen Martinalvarez, David Martinoliva, T Caballero, Paloma Rueda, Josefa LeonAbstract:Hepatocellular carcinoma (HCC) is associated with a poor prognosis due to a lack of effective treatment options. In HCC a significant role is played by DNA damage and the inflammatory response. Poly (ADP-ribose) polymerase-1 (PARP-1) is an important protein that regulates both these mechanisms. The objective of this study was to examine the effect of pharmacology PARP-1 inhibition on the reduction of tumor volume of HCC xenograft and on the hepatocarcinoGenesis induced by diethyl-nitrosamine (DEN). Pharmacologic PARP-1 inhibition with DPQ greatly reduces tumor xenograft volume with regard to a nontreated xenograft (394 mm3 versus 2,942 mm3, P < 0.05). This observation was paralleled by reductions in xenograft mitosis (P = 0.02) and tumor vasculoGenesis (P = 0.007, confirmed by in vitro angioGenesis study), as well as by an increase in the number of apoptotic cells in DPQ-treated mice (P = 0.04). A substantial difference in key Tumor-Related Gene expression (transformed 3T3 cell double minute 2 [MDM2], FLT1 [vascular endothelial growth factor receptor-1, VEGFR1], epidermal growth factor receptor [EPAS1]/hypoxia-inducible factor 2 [HIF2A], EGLN1 [PHD2], epidermal growth factor receptor [EGFR], MYC, JUND, SPP1 [OPN], hepatocyte growth factor [HGF]) was found between the control tumor xenografts and the PARP inhibitor-treated xenografts (data confirmed in HCC cell lines using PARP inhibitors and PARP-1 small interfering RNA [siRNA]). Furthermore, the results obtained in mice treated with DEN to induce hepatocarcinoGenesis showed, after treatment with a PARP inhibitor (DPQ), a significant reduction both in preneoplastic foci and in the expression of preneoplastic markers and proinflammatory Genes (Gstm3, Vegf, Spp1 [Opn], IL6, IL1b, and Tnf), bromodeoxyuridine incorporation, and NF-κB activation in the initial steps of carcinoGenesis (P < 0.05). Conclusion: This study shows that PARP inhibition is capable of controlling HCC growth and preventing tumor vasculoGenesis by regulating the activation of different Genes involved in tumor progression. (HEPATOLOGY 2010;51:255–266.)
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Inhibition of poly adenosine diphosphate‐ribose polymerase decreases hepatocellular carcinoma growth by modulation of tumor‐related Gene expression
Hepatology (Baltimore Md.), 2009Co-Authors: Rosa Quiles-pérez, T Caballero, Paloma Rueda, José Antonio Muñoz-gámez, Ángeles Ruiz-extremera, Francisco O'valle, Laura Sanjuan-nuñez, Ana Belén Martín‐Álvarez, David Martín-oliva, Josefa LeonAbstract:Hepatocellular carcinoma (HCC) is associated with a poor prognosis due to a lack of effective treatment options. In HCC a significant role is played by DNA damage and the inflammatory response. Poly (ADP-ribose) polymerase-1 (PARP-1) is an important protein that regulates both these mechanisms. The objective of this study was to examine the effect of pharmacology PARP-1 inhibition on the reduction of tumor volume of HCC xenograft and on the hepatocarcinoGenesis induced by diethyl-nitrosamine (DEN). Pharmacologic PARP-1 inhibition with DPQ greatly reduces tumor xenograft volume with regard to a nontreated xenograft (394 mm3 versus 2,942 mm3, P < 0.05). This observation was paralleled by reductions in xenograft mitosis (P = 0.02) and tumor vasculoGenesis (P = 0.007, confirmed by in vitro angioGenesis study), as well as by an increase in the number of apoptotic cells in DPQ-treated mice (P = 0.04). A substantial difference in key Tumor-Related Gene expression (transformed 3T3 cell double minute 2 [MDM2], FLT1 [vascular endothelial growth factor receptor-1, VEGFR1], epidermal growth factor receptor [EPAS1]/hypoxia-inducible factor 2 [HIF2A], EGLN1 [PHD2], epidermal growth factor receptor [EGFR], MYC, JUND, SPP1 [OPN], hepatocyte growth factor [HGF]) was found between the control tumor xenografts and the PARP inhibitor-treated xenografts (data confirmed in HCC cell lines using PARP inhibitors and PARP-1 small interfering RNA [siRNA]). Furthermore, the results obtained in mice treated with DEN to induce hepatocarcinoGenesis showed, after treatment with a PARP inhibitor (DPQ), a significant reduction both in preneoplastic foci and in the expression of preneoplastic markers and proinflammatory Genes (Gstm3, Vegf, Spp1 [Opn], IL6, IL1b, and Tnf), bromodeoxyuridine incorporation, and NF-κB activation in the initial steps of carcinoGenesis (P < 0.05). Conclusion: This study shows that PARP inhibition is capable of controlling HCC growth and preventing tumor vasculoGenesis by regulating the activation of different Genes involved in tumor progression. (HEPATOLOGY 2010;51:255–266.)
