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Your search keyword '"Huh, Nam-ho"' showing total 9 results
Start Over Author "Huh, Nam-ho" Journal cancer research
9 results on '"Huh, Nam-ho"'

1. Abstract 2879: Anti-cancer effects of REIC/Dkk-3-encoding adenoviral vector for the treatment of non-small cell lung cancer

Author

Suzawa, Ken, primary, Toyooka, Shinichi, additional, Shien, Kazuhiko, additional, Tanaka, Norimitsu, additional, Watanabe, Masami, additional, Soh, Junichi, additional, Sakaguchi, Masakiyo, additional, Matsuo, Keitaro, additional, Yamamoto, Hiromasa, additional, Furukawa, Masashi, additional, Asano, Hiroaki, additional, Tsukuda, Kazunori, additional, Nasu, Yasutomo, additional, Huh, Nam-Ho, additional, Miyoshi, Shinichiro, additional, and Kumon, Hiromi, additional

Published
2014
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4. Abstract 2081: Frequent silencing of tumor suppressive MicroRNA-34b/c by aberrant methylation in malignant mesothelioma

Author

Kubo, Takafumi, primary, Toyooka, Shinichi, additional, Tsukuda, Kazunori, additional, Asano, Hiroaki, additional, Sakaguchi, Masakiyo, additional, Soh, Junichi, additional, Ueno, Tsuyoshi, additional, Yamamoto, Hiromasa, additional, Yamane, Masaomi, additional, Oto, Takahiro, additional, Nasu, Yasutomo, additional, Matsui, Hideki, additional, Huh, Nam ho, additional, and Miyoshi, Shinichro, additional

Published
2010
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5. Abstract 1616: The anti-tumor effect of TAE226, dual inhibitor of FAK and IGF-IR, on non-small-cell lung cancer with EGFR mutation

Author

Otani, Hiroki, primary, Toyooka, Shinichi, additional, Takaoka, Munenori, additional, Sakaguchi, Masakiyo, additional, Ueno, Tsuyoshi, additional, Yamamoto, Hiromasa, additional, Soh, Junichi, additional, Kubo, Takafumi, additional, Asano, Hiroaki, additional, Tsukuda, Kazunori, additional, Yamane, Masaomi, additional, Oto, Takahiro, additional, Kiura, Katsuyuki, additional, Huh, Nam-ho, additional, Naomoto, Yoshio, additional, and Miyoshi, Shinichiro, additional

Published
2010
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6. Down-regulation of Inhibition of Differentiation-1 via Activation of Activating Transcription Factor 3 and Smad Regulates REIC/Dickkopf-3–Induced Apoptosis

Author

Kashiwakura, Yuji, primary, Ochiai, Kazuhiko, additional, Watanabe, Masami, additional, Abarzua, Fernando, additional, Sakaguchi, Masakiyo, additional, Takaoka, Munenori, additional, Tanimoto, Ryuta, additional, Nasu, Yasutomo, additional, Huh, Nam-ho, additional, and Kumon, Hiromi, additional

Published
2008
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9. Involvement of interferon regulatory factor 1 and S100C/A11 in growth inhibition by transforming growth factor beta 1 in human hepatocellular carcinoma cells.

Author

Miyazaki M, Sakaguchi M, Akiyama I, Sakaguchi Y, Nagamori S, and Huh NH

Subjects
Carcinoma, Hepatocellular drug therapy, Carcinoma, Hepatocellular genetics, Carcinoma, Hepatocellular metabolism, Cell Division drug effects, Cell Division physiology, Cell Line, Tumor, Cyclin-Dependent Kinase Inhibitor p21, Cyclins antagonists & inhibitors, Cyclins biosynthesis, DNA-Binding Proteins biosynthesis, Humans, Interferon Regulatory Factor-1, Liver Neoplasms drug therapy, Liver Neoplasms genetics, Liver Neoplasms metabolism, Phosphoproteins biosynthesis, RNA, Messenger biosynthesis, RNA, Messenger genetics, Reverse Transcriptase Polymerase Chain Reaction, S100 Proteins biosynthesis, Transforming Growth Factor beta1, Tumor Suppressor Protein p53 biosynthesis, Tumor Suppressor Protein p53 genetics, Carcinoma, Hepatocellular pathology, DNA-Binding Proteins physiology, Liver Neoplasms pathology, Phosphoproteins physiology, S100 Proteins physiology, Transforming Growth Factor beta pharmacology
Abstract

Growth inhibition by transforming growth factor (TGF)-beta 1 has been attributed to the induction of cyclin-dependent kinase inhibitors, among which p21/Waf1 plays a major role in many biological contexts. In the present study, two new intracellular mediators for the induction of p21/Waf1 by TGF-beta 1 were identified in a human hepatocellular carcinoma cell line (JHH-5) expressing mutant-type p53. After addition of TGF-beta 1 to JHH-5 cells, a marked increase of the p21/Waf1 expression preceded the inhibition of DNA synthesis. Expression of IFN regulatory factor (IRF)-1, a known transacting factor for p21/Waf1 promoter, was elevated just before or in parallel with the increase of p21/Waf1. Transduction of antisense IRF-1 inhibited the increase in p21/Waf1 in JHH-5 cells treated with TGF-beta 1 and partially released the cells from the growth arrest by TGF-beta 1. Expression of S100C/A11, a member of the Ca(2+)-binding S100 protein family, also markedly increased after addition of TGF-beta 1. S100C/A11 protein was translocated to and accumulated in nuclei of TGF-beta 1-treated JHH-5 cells, where p21/Waf1 was concomitantly accumulated. When a recombinant S100C/A11 protein was introduced into nuclei of JHH-5 cells, DNA synthesis was markedly inhibited in a dose-dependent manner in the absence of TGF-beta 1. Prior transfection of p21/Waf1-targeted small interfering RNA efficiently blocked decrease of DNA synthesis in JHH-5 cells caused by TAT-S100C/A11 or TGF-beta 1 and markedly inhibited expression of p21/Waf1 protein in the cells. These results indicate that IRF-1 and S100C/A11 mediate growth inhibition by TGF-beta 1 via induction of p21/Waf1.

Published
2004
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