The Experts below are selected from a list of 183 Experts worldwide ranked by ideXlab platform
Inpyo Choi - One of the best experts on this subject based on the ideXlab platform.
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VDUP1 upregulated by TGF-β1 and 1,25-dihydorxyvitamin D_3 inhibits tumor cell growth by blocking cell-cycle progression
Oncogene, 2003Co-Authors: Jun Ho Jeon, Hyang Ran Ju, Uhee Jung, Kyu Sang Song, Ho Myeung Hwang, Yoon Sook Na, Young Yang, Inpyo ChoiAbstract:Vitamin D_3 upregulated protein 1 (VDUP1) is a 1,25-dihydroxyvitamin D_3 (1,25(OH)_2D_3) upregulated protein, and it is induced by various stresses. In human tumor tissues, VDUP1 expression was downregulated. Upon stimulation by growth-inhibitory signals such as TGF- β 1 and 1,25(OH)_2D_3, its expression was rapidly upregulated as the cell growth was retarded. The transfection of VDUP1 in tumor cells reduced cell growth. The VDUP1 expression was also increased when the cell-cycle progression was arrested. Transfection of VDUP1 induced cell-cycle arrest at the G0/G1 phase, indicating that VDUP1 possesses a tumor-suppressive activity. In addition, it was found that VDUP1 interacted with promyelocytic leukemia zinc-finger, Fanconi anemia zinc-finger, and histone deacetylase 1, which are known to be transcriptional corepressors. VDUP1 itself suppressed IL-3 receptor and cyclin A2 promoter activity. Taken together, these results suggest that VDUP1 is a novel Antitumor Gene which forms a transcriptional repressor complex.
Jun Ho Jeon - One of the best experts on this subject based on the ideXlab platform.
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VDUP1 upregulated by TGF-β1 and 1,25-dihydorxyvitamin D_3 inhibits tumor cell growth by blocking cell-cycle progression
Oncogene, 2003Co-Authors: Jun Ho Jeon, Hyang Ran Ju, Uhee Jung, Kyu Sang Song, Ho Myeung Hwang, Yoon Sook Na, Young Yang, Inpyo ChoiAbstract:Vitamin D_3 upregulated protein 1 (VDUP1) is a 1,25-dihydroxyvitamin D_3 (1,25(OH)_2D_3) upregulated protein, and it is induced by various stresses. In human tumor tissues, VDUP1 expression was downregulated. Upon stimulation by growth-inhibitory signals such as TGF- β 1 and 1,25(OH)_2D_3, its expression was rapidly upregulated as the cell growth was retarded. The transfection of VDUP1 in tumor cells reduced cell growth. The VDUP1 expression was also increased when the cell-cycle progression was arrested. Transfection of VDUP1 induced cell-cycle arrest at the G0/G1 phase, indicating that VDUP1 possesses a tumor-suppressive activity. In addition, it was found that VDUP1 interacted with promyelocytic leukemia zinc-finger, Fanconi anemia zinc-finger, and histone deacetylase 1, which are known to be transcriptional corepressors. VDUP1 itself suppressed IL-3 receptor and cyclin A2 promoter activity. Taken together, these results suggest that VDUP1 is a novel Antitumor Gene which forms a transcriptional repressor complex.
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VDUP1 upregulated by TGF-β1 and 1,25-dihydorxyvitamin D3 inhibits tumor cell growth by blocking cell-cycle progression
Oncogene, 2003Co-Authors: Jun Ho Jeon, Hyang Ran Ju, Uhee Jung, Kyu Sang Song, Ho Myeung Hwang, Yoon Sook NaAbstract:Vitamin D3 upregulated protein 1 (VDUP1) is a 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) upregulated protein, and it is induced by various stresses. In human tumor tissues, VDUP1 expression was downregulated. Upon stimulation by growth-inhibitory signals such as TGF-β1 and 1,25(OH)2D3, its expression was rapidly upregulated as the cell growth was retarded. The transfection of VDUP1 in tumor cells reduced cell growth. The VDUP1 expression was also increased when the cell-cycle progression was arrested. Transfection of VDUP1 induced cell-cycle arrest at the G0/G1 phase, indicating that VDUP1 possesses a tumor-suppressive activity. In addition, it was found that VDUP1 interacted with promyelocytic leukemia zinc-finger, Fanconi anemia zinc-finger, and histone deacetylase 1, which are known to be transcriptional corepressors. VDUP1 itself suppressed IL-3 receptor and cyclin A2 promoter activity. Taken together, these results suggest that VDUP1 is a novel Antitumor Gene which forms a transcriptional repressor complex.
Yoon Sook Na - One of the best experts on this subject based on the ideXlab platform.
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VDUP1 upregulated by TGF-β1 and 1,25-dihydorxyvitamin D_3 inhibits tumor cell growth by blocking cell-cycle progression
Oncogene, 2003Co-Authors: Jun Ho Jeon, Hyang Ran Ju, Uhee Jung, Kyu Sang Song, Ho Myeung Hwang, Yoon Sook Na, Young Yang, Inpyo ChoiAbstract:Vitamin D_3 upregulated protein 1 (VDUP1) is a 1,25-dihydroxyvitamin D_3 (1,25(OH)_2D_3) upregulated protein, and it is induced by various stresses. In human tumor tissues, VDUP1 expression was downregulated. Upon stimulation by growth-inhibitory signals such as TGF- β 1 and 1,25(OH)_2D_3, its expression was rapidly upregulated as the cell growth was retarded. The transfection of VDUP1 in tumor cells reduced cell growth. The VDUP1 expression was also increased when the cell-cycle progression was arrested. Transfection of VDUP1 induced cell-cycle arrest at the G0/G1 phase, indicating that VDUP1 possesses a tumor-suppressive activity. In addition, it was found that VDUP1 interacted with promyelocytic leukemia zinc-finger, Fanconi anemia zinc-finger, and histone deacetylase 1, which are known to be transcriptional corepressors. VDUP1 itself suppressed IL-3 receptor and cyclin A2 promoter activity. Taken together, these results suggest that VDUP1 is a novel Antitumor Gene which forms a transcriptional repressor complex.
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VDUP1 upregulated by TGF-β1 and 1,25-dihydorxyvitamin D3 inhibits tumor cell growth by blocking cell-cycle progression
Oncogene, 2003Co-Authors: Jun Ho Jeon, Hyang Ran Ju, Uhee Jung, Kyu Sang Song, Ho Myeung Hwang, Yoon Sook NaAbstract:Vitamin D3 upregulated protein 1 (VDUP1) is a 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) upregulated protein, and it is induced by various stresses. In human tumor tissues, VDUP1 expression was downregulated. Upon stimulation by growth-inhibitory signals such as TGF-β1 and 1,25(OH)2D3, its expression was rapidly upregulated as the cell growth was retarded. The transfection of VDUP1 in tumor cells reduced cell growth. The VDUP1 expression was also increased when the cell-cycle progression was arrested. Transfection of VDUP1 induced cell-cycle arrest at the G0/G1 phase, indicating that VDUP1 possesses a tumor-suppressive activity. In addition, it was found that VDUP1 interacted with promyelocytic leukemia zinc-finger, Fanconi anemia zinc-finger, and histone deacetylase 1, which are known to be transcriptional corepressors. VDUP1 itself suppressed IL-3 receptor and cyclin A2 promoter activity. Taken together, these results suggest that VDUP1 is a novel Antitumor Gene which forms a transcriptional repressor complex.
Yigang Wang - One of the best experts on this subject based on the ideXlab platform.
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Oncolytic adenovirus expressing ST13 increases Antitumor effect of TRAIL against pancreatic ductal adenocarcinoma.
Human gene therapy, 2020Co-Authors: Youni Zhang, Shibing Wang, Fang Huang, Miaojuan Ye, Huiju Wang, Yigang WangAbstract:Oncolytic adenoviruses are promising agents for cancer therapy and providing a new therapeutic strategy for pancreatic ductal adenocarcinoma (PDAC) Gene therapy. However, the challenges associated with the therapeutic effect of oncolytic adenovirus alone include security of virus vector and screening of effective Antitumor Gene. In this study, a novel oncolytic adenovirus CD55-ST13-TRAIL was constructed featured with CEA promoter to control E1A, and E1B 55 kDa Gene deletion in which dual therapeutic Gene ST13 and TRAIL was inserted. ST13, firstly as a colorectal cancer suppressor Gene, was also lower expression in PDAC than in tumor-adjacent tissues, which was associated with poor prognosis of PDAC patients. In vitro studies showed that CD55-ST13-TRAIL can efficiently proliferate and promote the expression of ST13 and TRAIL in CEA positive pancreatic cancer cells. Moreover, CD55-ST13-TRAIL has a synergic cell-killing effect compared with CD55-ST13 alone or CD55-TRAIL alone, and the inhibition of PDAC cell metastasis and promotion of apoptosis by triggering EMT and apoptotic pathways in PDAC cells. Further xenograft experiments in mice model indicated that CD55-ST13-TRAIL significantly inhibited tumor growth and improved the survival rates of xenograft animal. The findings demonstrated that the oncolytic virotherapy under the control of CEA promoter enables the treatment safety and efficiency to PDAC, which makes it a promising candidate for the treatment of metastatic diseases.
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Targeting Gene-Virus-Mediated Manganese Superoxide Dismutase Effectively Suppresses Tumor Growth in Hepatocellular Carcinoma In Vitro and In Vivo
Cancer Biotherapy and Radiopharmaceuticals, 2014Co-Authors: Fang Huang, Yigang Wang, Buyun Ma, Ruijuan Xiao, Yanping Kong, Xiumei ZhouAbstract:Abstract Although the treatment methods for hepatocellular carcinoma (HCC) have made a great progress on patient survival rate and life quality, the HCC recurrence still is very high. To explore the novel effective anticancer strategies for HCC, the Cancer Targeting Gene-Viro-Therapy (CTGVT) strategy was applied through oncolytic virus-delivery Antitumor Gene. In this article, the dual-regulated oncolytic adenovirus Ad-AFP-E1A-E1B(Δ55kDa)-Mn-SOD (briefly named AD55-Mn-SOD) was constructed using a liver cancer-specific α-fetoprotein (AFP) promoter to control replication-essential E1A Gene and deliver the novel tumor suppression Gene Manganese superoxide dismutase (Mn-SOD). The results indicated that the constructed AD55-Mn-SOD exerted tumor-specific features, and induced dramatic cytotoxicity in HCC cells in vitro and suppress the HCC xenografted growth in nude mice. Moreover, the anticancer mechanism of AD55-Mn-SOD is due to the activation of caspase apoptotic pathway. These data suggested that AD55-Mn-SO...
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potent and specific Antitumor effect for colorectal cancer by cea and rb double regulated oncolytic adenovirus harboring st13 Gene
PLOS ONE, 2012Co-Authors: Xiumei Zhou, Shibing Wang, Yigang Wang, Kangjian Zhang, Shu Zheng, Lianli Xiao, Yuemei Yu, Yue ZhangAbstract:Cancer Targeting Gene-Viro-Therapy (CTGVT) is constructed by inserting an Antitumor Gene into an oncolytic virus (OV). It is actually an OV-Gene therapy, which has much better Antitumor effect than either Gene therapy alone or virotherapy alone in our previously published papers. This study is a modification of CTGVT by inserting a colorectal cancer (CRC) specific suppressor Gene, ST13, into a CRC specific oncolytic virus, the Ad·CEA·E1A(Δ24), to construct the Ad·(ST13)·CEA·E1A(Δ24) for increasing the targeting tropism to colorectal cancer and it was briefly named as CTGVT-CRC. Although many studies on CEA promoter and ST13 Gene were reported but no construct has been performed to combine both of them as a new strategy for colorectal cancer (CRC) specific therapy. In addition to the CRC specificity, the Antitumor effect of Ad·(ST13)·CEA·E1A(Δ24) was also excellent and got nearly complete inhibition (not eradication) of CRC xenograft since ST13 was an effective Antitumor Gene with less toxicity, and a Chinese patent (No. 201110319434.4) was available for this study. Ad·(ST13)·CEA·E1A(Δ24) caused cell apoptosis through P38 MAPK (i.e. P38) which upregulated CHOP and ATF2 expression. The mitochondrial medicated apoptosis pathway was activated by the increase of caspase 9 and caspase 3 expression.
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722. Antitumor Effect of IL-24 Mediated by Tumor Targeting Vector ZD55 Is Much Better Than That Mediated by Replication Deficient Adenovirus
Molecular Therapy, 2005Co-Authors: Li Li Zhao, Yigang Wang, Jin Fa Gu, Zi Lai Zhang, Qi Jun Qian, Yan Hong Zhang, Aiwen Dong, Ling Feng He, Jin-he Zhang, Cheng QianAbstract:It has been demonstrated that interleukin-24 (also called melanoma differentiation associated Gene-7, mda-7), exerts Antitumor effect mediated by replicative deficient adenovirus. But the Antitumor effect of Ad-IL-24 is limited. In this study, a targeting and replication adenovirus vector ZD55 was used which was similar to ONYX-015 but with marked difference in its construction method, especially with a cloning site to insert foreign Antitumor Gene. The ZD55-IL-24 could express substantially more IL-24 than Ad-Il-24 due to the replicate property of ZD55 and showed significant apoptosis for Antitumor effect due to its additional targeting effect to p53 negative tumor. Therefore, ZD55-IL-24 could have more anitumor effect in vitro or in vivo than either ONYX-015 or Ad-IL-24, but no or very lower cytotoxic and apoptotic effect in normal cells. The Antitumor effect of ZD55-IL-24 is excellent with 1/3 experimental mice perfect free from tumor and the rest mice bore very small tumor mass, showing the potent Antitumor activity of ZD55-IL-24 which might have practical meanings and provide new protocol for cancer therapy. This is the first repot of Antitumor effect of IL-24 in a targeting and replicate vector as ZD55. Furthermore, one of the mechanism of Antitumor effect from ZD55-IL-24 was confirmed to be due to the apoptosis by the induction expression of Caspase 3, 9 and its clevation for activation. Cytochome C and Bax were also increased showing this apoptosis might relate to the mitochondrial pathway.
Y-z Du - One of the best experts on this subject based on the ideXlab platform.
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Effective Antitumor Gene therapy delivered by polyethylenimine-conjugated stearic acid-g-chitosan oligosaccharide micelles
Gene Therapy, 2013Co-Authors: F-q Hu, W-w Chen, M-d Zhao, H Yuan, Y-z DuAbstract:Non-viral vesicle composing of low-molecular weight polyethylenimine-conjugated stearic acid-g-chitosan oligosaccharide (CSOSA-g-PEI) was synthesized for Gene delivery and therapy. The synthesized CSOSA-g-PEI had good ion-buffer capabilities and DNA-binding capacity, which could form positively charged nano-sized particles (100–150 nm) with plasmid DNA; in vitro Gene transfection tests demonstrated that CSOSA-g-PEI presented much lower cytotoxicity and corresponding transfection efficiency in comparison with Lipofectamine 2000 in both human cancer cells (Hela and MCF-7). The Gene transfection of CSOSA-g-PEI/pDNA could be further enhanced in the presence of serum or by adding arginine during incubation of CSOSA-g-PEI micelles with plasmid DNA. The biodistribution experiments demonstrated CSOSA-g-PEI conjugate highly localized in the tumor tissue and indicated a persistently increased accumulation. In vivo Antitumor activity results showed that CSOSA-g-PEI/plasmid pigment epithelium-derived factor formulation could effectively suppress the tumor growth (above 60% tumor inhibition) without systematic toxicity against animal body after intravenous injection.
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Effective Antitumor Gene therapy delivered by polyethylenimine-conjugated stearic acid-g-chitosan oligosaccharide micelles
Gene Therapy, 2012Co-Authors: F-q Hu, W-w Chen, M-d Zhao, H Yuan, Y-z DuAbstract:Effective Antitumor Gene therapy delivered by polyethylenimine-conjugated stearic acid-g-chitosan oligosaccharide micelles
