The Experts below are selected from a list of 5583 Experts worldwide ranked by ideXlab platform
Tachung Chao - One of the best experts on this subject based on the ideXlab platform.
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in vivo growth suppression of ct 26 mouse colorectal cancer cells by adenovirus expressed Small Hairpin RNA specifically targeting thymosin beta 4 mRNA
Cancer Gene Therapy, 2014Co-Authors: Tachung Chao, Lichuan Chan, S Y Ju, M C Tang, Pomin Chen, Chenghwai Tzeng, Yeu SuAbstract:In vivo growth suppression of CT-26 mouse colorectal cancer cells by adenovirus-expressed Small Hairpin RNA specifically targeting thymosin beta-4 mRNA
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In vivo growth suppression of CT-26 mouse colorectal cancer cells by adenovirus-expressed Small Hairpin RNA specifically targeting thymosin beta-4 mRNA
Cancer Gene Therapy, 2014Co-Authors: Tachung Chao, Lichuan Chan, Pomin Chen, Chenghwai Tzeng, Ju Sy, Tang Mc, Yeu SuAbstract:Thymosin beta-4 (Tβ4) is known to be involved in tumorigenesis. Overexpression of this polypeptide has been observed in a wide variety of cancers, including colorectal carcinoma (CRC). Accordingly, Tβ4 has been proposed to be a novel therapeutic target for CRC, especially in its metastatic form. Although in vitro tumor-suppressive effects of Tβ4 gene silencing mediated by Small Hairpin RNA (shRNA) have already been demonstrated, the in vivo efficacy of such an approach has not yet been reported. Herein, we demonstrated that infection with recombinant adenovirus expressing an shRNA targeting Tβ4 markedly reduced the growth of and robustly induced apoptosis in CT-26 mouse CRC cells in culture. Additionally, tumors grown in nude mice from the CT-26 cells whose Tβ4 expression already been downregulated by virus infection were also drastically reduced. Most importantly, significant growth arrest of tumors derived from the parental CT-26 cells was observed after multiple intratumoral injections of these viruses. Together, our results show for the first time that in vivo silencing of Tβ4 expression by its shRNA generated after adenoviral infection can suppress CRC growth. These results further demonstrate the feasibility of treating CRC by a Tβ4 knockdown gene therapeutic approach.
Yeu Su - One of the best experts on this subject based on the ideXlab platform.
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in vivo growth suppression of ct 26 mouse colorectal cancer cells by adenovirus expressed Small Hairpin RNA specifically targeting thymosin beta 4 mRNA
Cancer Gene Therapy, 2014Co-Authors: Tachung Chao, Lichuan Chan, S Y Ju, M C Tang, Pomin Chen, Chenghwai Tzeng, Yeu SuAbstract:In vivo growth suppression of CT-26 mouse colorectal cancer cells by adenovirus-expressed Small Hairpin RNA specifically targeting thymosin beta-4 mRNA
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In vivo growth suppression of CT-26 mouse colorectal cancer cells by adenovirus-expressed Small Hairpin RNA specifically targeting thymosin beta-4 mRNA
Cancer Gene Therapy, 2014Co-Authors: Tachung Chao, Lichuan Chan, Pomin Chen, Chenghwai Tzeng, Ju Sy, Tang Mc, Yeu SuAbstract:Thymosin beta-4 (Tβ4) is known to be involved in tumorigenesis. Overexpression of this polypeptide has been observed in a wide variety of cancers, including colorectal carcinoma (CRC). Accordingly, Tβ4 has been proposed to be a novel therapeutic target for CRC, especially in its metastatic form. Although in vitro tumor-suppressive effects of Tβ4 gene silencing mediated by Small Hairpin RNA (shRNA) have already been demonstrated, the in vivo efficacy of such an approach has not yet been reported. Herein, we demonstrated that infection with recombinant adenovirus expressing an shRNA targeting Tβ4 markedly reduced the growth of and robustly induced apoptosis in CT-26 mouse CRC cells in culture. Additionally, tumors grown in nude mice from the CT-26 cells whose Tβ4 expression already been downregulated by virus infection were also drastically reduced. Most importantly, significant growth arrest of tumors derived from the parental CT-26 cells was observed after multiple intratumoral injections of these viruses. Together, our results show for the first time that in vivo silencing of Tβ4 expression by its shRNA generated after adenoviral infection can suppress CRC growth. These results further demonstrate the feasibility of treating CRC by a Tβ4 knockdown gene therapeutic approach.
Xinsong Li - One of the best experts on this subject based on the ideXlab platform.
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Galactosylated 2-hydroxypropyl methacrylamide-s-3-guanidinopropyl methacrylamide copolymer as a Small Hairpin RNA carrier for inhibiting human telomerase reverse transcriptase expression.
Journal of Gene Medicine, 2014Co-Authors: Yang Wu, Jingkai Ji, Ran Yang, Xiaoqiang Zhang, Yuanhui Li, Yuepu Pu, Xinsong LiAbstract:BACKGROUND: In the present study, a well-defined glucose and guanidine based copolymer, galactosylated 2-hydroxypropyl methacrylamide-s-3-guanidinopropyl methacrylamide (HPMA-s-GPMA) abbreviated as GGH was prepared and self-assembled with Small Hairpin RNA (shRNA) to inhibit human telomerase reverse transcriptase (hTERT) gene expression in vitro to develop a shRNA carrier. METHODS: First, HPMA-s-APMA copolymers were synthesized by aqueous reversible addition-fragmentation chain transfer polymerization, followed by galactosylation and guanidinylation. Then, three target shRNAs containing green fluorescent protein gene as a reporter were combined with GGH to form shRNA/GGH polyplexes. RESULTS: GGH copolymers could condense shRNA to form shRNA/GGH polyplex particles with a diameter in the range 122.8-331.6 nm in phosphate-buffered saline, and zeta potential values ranging from +3.7 to +16.5 mV at various charge ratios (N/P). That the cytotoxicity of GGH copolymers was significantly lower than that of PEI in human hepatocellular liver carcinoma cells (HepG2) and human cervix epithelial carcinoma cells. The transfection efficiency of shRNA/GGH polyplexes was higher than that of PEI at a charge ratio of 12 in the HepG2 cell line. Furthermore, shRNA/GGH polyplexes could effectively silence hTERT mRNA expression in serum-free medium (p
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galactosylated 2 hydroxypropyl methacrylamide s 3 guanidinopropyl methacrylamide copolymer as a Small Hairpin RNA carrier for inhibiting human telomerase reverse transcriptase expression
Journal of Gene Medicine, 2014Co-Authors: Yang Wu, Jingkai Ji, Ran Yang, Xiaoqiang Zhang, Yuanhui Li, Yuepu Pu, Xinsong LiAbstract:BACKGROUND: In the present study, a well-defined glucose and guanidine based copolymer, galactosylated 2-hydroxypropyl methacrylamide-s-3-guanidinopropyl methacrylamide (HPMA-s-GPMA) abbreviated as GGH was prepared and self-assembled with Small Hairpin RNA (shRNA) to inhibit human telomerase reverse transcriptase (hTERT) gene expression in vitro to develop a shRNA carrier. METHODS: First, HPMA-s-APMA copolymers were synthesized by aqueous reversible addition-fragmentation chain transfer polymerization, followed by galactosylation and guanidinylation. Then, three target shRNAs containing green fluorescent protein gene as a reporter were combined with GGH to form shRNA/GGH polyplexes. RESULTS: GGH copolymers could condense shRNA to form shRNA/GGH polyplex particles with a diameter in the range 122.8-331.6 nm in phosphate-buffered saline, and zeta potential values ranging from +3.7 to +16.5 mV at various charge ratios (N/P). That the cytotoxicity of GGH copolymers was significantly lower than that of PEI in human hepatocellular liver carcinoma cells (HepG2) and human cervix epithelial carcinoma cells. The transfection efficiency of shRNA/GGH polyplexes was higher than that of PEI at a charge ratio of 12 in the HepG2 cell line. Furthermore, shRNA/GGH polyplexes could effectively silence hTERT mRNA expression in serum-free medium (p < 0.01) and decrease the aggregation of protein in the medium with the presence of 10% serum. In addition, hTERT mRNA expression in HepG2 cells demosntrate a significant difference between siRNA/GGH polyplexes and blank samples (p < 0.05). CONCLUSIONS: GGH copolymers could integrate advantages relating to galactose content for hepatocyte targeting, guanidino groups for cell penetration and HPMA component for shielding, showing great potential for effective hepatocyte targeting gene delivery.
Lichuan Chan - One of the best experts on this subject based on the ideXlab platform.
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in vivo growth suppression of ct 26 mouse colorectal cancer cells by adenovirus expressed Small Hairpin RNA specifically targeting thymosin beta 4 mRNA
Cancer Gene Therapy, 2014Co-Authors: Tachung Chao, Lichuan Chan, S Y Ju, M C Tang, Pomin Chen, Chenghwai Tzeng, Yeu SuAbstract:In vivo growth suppression of CT-26 mouse colorectal cancer cells by adenovirus-expressed Small Hairpin RNA specifically targeting thymosin beta-4 mRNA
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In vivo growth suppression of CT-26 mouse colorectal cancer cells by adenovirus-expressed Small Hairpin RNA specifically targeting thymosin beta-4 mRNA
Cancer Gene Therapy, 2014Co-Authors: Tachung Chao, Lichuan Chan, Pomin Chen, Chenghwai Tzeng, Ju Sy, Tang Mc, Yeu SuAbstract:Thymosin beta-4 (Tβ4) is known to be involved in tumorigenesis. Overexpression of this polypeptide has been observed in a wide variety of cancers, including colorectal carcinoma (CRC). Accordingly, Tβ4 has been proposed to be a novel therapeutic target for CRC, especially in its metastatic form. Although in vitro tumor-suppressive effects of Tβ4 gene silencing mediated by Small Hairpin RNA (shRNA) have already been demonstrated, the in vivo efficacy of such an approach has not yet been reported. Herein, we demonstrated that infection with recombinant adenovirus expressing an shRNA targeting Tβ4 markedly reduced the growth of and robustly induced apoptosis in CT-26 mouse CRC cells in culture. Additionally, tumors grown in nude mice from the CT-26 cells whose Tβ4 expression already been downregulated by virus infection were also drastically reduced. Most importantly, significant growth arrest of tumors derived from the parental CT-26 cells was observed after multiple intratumoral injections of these viruses. Together, our results show for the first time that in vivo silencing of Tβ4 expression by its shRNA generated after adenoviral infection can suppress CRC growth. These results further demonstrate the feasibility of treating CRC by a Tβ4 knockdown gene therapeutic approach.
Pomin Chen - One of the best experts on this subject based on the ideXlab platform.
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in vivo growth suppression of ct 26 mouse colorectal cancer cells by adenovirus expressed Small Hairpin RNA specifically targeting thymosin beta 4 mRNA
Cancer Gene Therapy, 2014Co-Authors: Tachung Chao, Lichuan Chan, S Y Ju, M C Tang, Pomin Chen, Chenghwai Tzeng, Yeu SuAbstract:In vivo growth suppression of CT-26 mouse colorectal cancer cells by adenovirus-expressed Small Hairpin RNA specifically targeting thymosin beta-4 mRNA
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In vivo growth suppression of CT-26 mouse colorectal cancer cells by adenovirus-expressed Small Hairpin RNA specifically targeting thymosin beta-4 mRNA
Cancer Gene Therapy, 2014Co-Authors: Tachung Chao, Lichuan Chan, Pomin Chen, Chenghwai Tzeng, Ju Sy, Tang Mc, Yeu SuAbstract:Thymosin beta-4 (Tβ4) is known to be involved in tumorigenesis. Overexpression of this polypeptide has been observed in a wide variety of cancers, including colorectal carcinoma (CRC). Accordingly, Tβ4 has been proposed to be a novel therapeutic target for CRC, especially in its metastatic form. Although in vitro tumor-suppressive effects of Tβ4 gene silencing mediated by Small Hairpin RNA (shRNA) have already been demonstrated, the in vivo efficacy of such an approach has not yet been reported. Herein, we demonstrated that infection with recombinant adenovirus expressing an shRNA targeting Tβ4 markedly reduced the growth of and robustly induced apoptosis in CT-26 mouse CRC cells in culture. Additionally, tumors grown in nude mice from the CT-26 cells whose Tβ4 expression already been downregulated by virus infection were also drastically reduced. Most importantly, significant growth arrest of tumors derived from the parental CT-26 cells was observed after multiple intratumoral injections of these viruses. Together, our results show for the first time that in vivo silencing of Tβ4 expression by its shRNA generated after adenoviral infection can suppress CRC growth. These results further demonstrate the feasibility of treating CRC by a Tβ4 knockdown gene therapeutic approach.