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Your search keyword '"Nakata, Daichi"' showing total 16 results
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16 results on '"Nakata, Daichi"'

7. Effects of epidermal growth factor (EGF) on invasive and metastatic potential of rat regressor tumor cell ER-1. Part 3. Oxidative stress and the induction of genomic instability by long-term EGF treatment.

Author

NAKATA, Daichi, primary, SHIBATA, Toshiyuki, additional, NAGAYASU, Hiroki, additional, KAWANO, Takashi, additional, KITAJYO, Hiroyuki, additional, AOYAMA, Tetsuya, additional, KOBAYASHI, Tokushige, additional, and ARISUE, Makoto, additional

Published
2000
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8. A functional and quantitative mutational analysis ofp53 mutations in yeast indicates strand biases and different roles of mutations in DMBA- and BBN-induced tumors in rats

Author

Yamamoto, Kazuhisa, primary, Nakata, Daichi, additional, Tada, Mitsuhiro, additional, Tonoki, Hidefumi, additional, Nishida, Takashi, additional, Hirai, Atsuko, additional, Ba, Yi, additional, Aoyama, Tetsuya, additional, Hamada, Jun-ichi, additional, Furuuchi, Keiji, additional, Harada, Hiroshi, additional, Hirai, Kei, additional, Shibahara, Nobuhisa, additional, Katsuoka, Yoji, additional, and Moriuchi, Tetsuya, additional

Published
1999
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15. A functional and quantitative mutational analysis of <TOGGLE>p53</TOGGLE> mutations in yeast indicates strand biases and different roles of mutations in DMBA- and BBN-induced tumors in rats

Author

Yamamoto, Kazuhisa, Nakata, Daichi, Tada, Mitsuhiro, Tonoki, Hidefumi, Nishida, Takashi, Hirai, Atsuko, Ba, Yi, Aoyama, Tetsuya, Hamada, Jun-ichi, Furuuchi, Keiji, Harada, Hiroshi, Hirai, Kei, Shibahara, Nobuhisa, Katsuoka, Yoji, and Moriuchi, Tetsuya

Abstract

In order to analyze the mutational events and to understand the biological significance of the p53 gene in chemical carcinogenesis, we applied a new yeast-based p53 functional assay to ovarian tumors induced by 7, 12-dimethylbenz[a]anthracene (DMBA), as well as to transitional cell carcinomas of the urinary bladder induced by N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN) in rats. The assay demonstrated that 15 of 19 DMBA induced tumors harbored clonal p53 mutations, which is consistent with the expectations of the “clonal expansion” hypothesis. The majority of the mutations were purine (AG) to pyrimidine (CT) transversions (12/19) on the non-transcribed (sense) strand (NTS), which is likely to be due to depurination created by DMBA adduct formation on the NTS. In contrast, we found no purine to pyrimidine transversion on the NTS. After cessation of BBN treatment, BBN-induced multifocal lesions in the bladder contained heterogeneous p53 mutations at an early stage. In the later stage, however, clonal p53 mutations were identified in 4 out of 7 bladders analyzed, conforming with the concept of “field cancerization”. The observed base substitutions were G→A (1/6) or C →T transitions (2/6), and mutations at T (3/6) on the NTS in clonal mutations, together with non-clonal mutations, showing a preference of C→T to G→A (17 vs. 0). Thus, preferential repair was found in the transcribed strand of the p53 gene, whether modified by DMBA or by BBN carcinogens. Very similar mutation patterns were observed between clonal and non-clonal mutations in the DMBA- and BBN-induced tumors, indicating that the rat yeast p53 functional assay can be a potential tool for the characterization of in vivo mutation patterns of p53, when modified by chemical carcinogens. Int. J. Cancer 83:700-705, 1999. © 1999 Wiley-Liss, Inc.

Published
1999
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16. Enhancement of tumorigenic, metastatic and in vitro invasive capacity of rat mammary tumor cells by transforming growth factor-beta.

Author

Nakata D, Hamada Ji, Ba Y, Matsushita K, Shibata T, Hosokawa M, and Moriuchi T

Subjects
Animals, Antibodies pharmacology, Cell Adhesion drug effects, Cell Adhesion Molecules genetics, Cell Movement drug effects, Chemotaxis drug effects, DNA-Binding Proteins, Dose-Response Relationship, Drug, Female, Hyaluronan Receptors immunology, Hyaluronic Acid pharmacology, Hyaluronoglucosaminidase pharmacology, Immediate-Early Proteins genetics, Kinetics, Mice, Neoplasm Invasiveness, Nuclear Proteins genetics, Trans-Activators genetics, Mammary Neoplasms, Experimental pathology, Neoplasm Metastasis pathology, Transforming Growth Factor beta pharmacology, Xenopus Proteins
Abstract

We investigated the effects of transforming growth factor-beta (TGF-beta) on biological behavior of a weakly malignant rat mammary carcinoma ER-1 cell line. TGF-beta enhanced the tumorigenic and metastatic capacity of ER-1 cells and their in vitro invasiveness to rat mesothelial and endothelial cell. Further cell biological analysis indicated that the increased invasive and metastatic capacity of ER-1 cells by TGF-beta was due to the increase in cell motility and adhesion to the mesothelial and endothelial cell monolayers. Thus, it is suggested that TGF-beta acts on ER-1 cells as a progression-enhancing factor which stimulates their adhesive and motile activities.

Published
2002
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