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Your search keyword '"KAWAMURA, Juichi"' showing total 6 results
Start Over Author "KAWAMURA, Juichi" Journal international journal of cancer
6 results on '"KAWAMURA, Juichi"'

2. Impact of genetic polymorphisms of 17-hydroxylase cytochrome P-450(CYP17) and steroid 5?-reductase type II(SRD5A2) genes on prostate-cancer risk among the Japanese population

Author

Yamada, Yasushi, primary, Watanabe, Masatoshi, additional, Murata, Mariko, additional, Yamanaka, Mikio, additional, Kubota, Yoshinobu, additional, Ito, Haruo, additional, Katoh, Takahiko, additional, Kawamura, Juichi, additional, Yatani, Ryuichi, additional, and Shiraishi, Taizo, additional

Published
2001
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5. Impact of genetic polymorphisms of 17-hydroxylase cytochrome P-450 <TOGGLE>(CYP17)</TOGGLE> and steroid 5α-reductase type II (SRD5A2) genes on prostate-cancer risk among the Japanese population

Author

Yamada, Yasushi, Watanabe, Masatoshi, Murata, Mariko, Yamanaka, Mikio, Kubota, Yoshinobu, Ito, Haruo, Katoh, Takahiko, Kawamura, Juichi, Yatani, Ryuichi, and Shiraishi, Taizo

Abstract

Steroid hormones, especially testosterone, play important roles in the carcinogenesis of prostate cancer, and several studies have reported changes in risk with polymorphisms of genes involved in steroid metabolism. One example is the CYP17 gene, which has a polymorphic T-to-C substitution in the 5'-untranslated region giving rise to A1 (T) and A2 (C) alleles. Steroid 5α-reductase type II (SRD5A2), which converts testosterone to the metabolically more active dihydrotestosterone, exhibits 2 polymorphisms: V89L, which substitutes leucine for valine at codon 89, and A49T, which substitutes threonine for alanine at codon 49. We therefore designed a case-control study of 105 prostate-cancer patients and 210 controls with benign prostatic hyperplasia for the purpose of investigating the association between prostate-cancer risk and polymorphisms in the SRD5A2 and CYP17 genes among the Japanese. The frequency of the CYP17 A2/A2 genotype in cases (18.8%) was higher than in controls (14.5%). Compared with the A1/A1 genotype, the odds ratio for the A2/A2 genotype was 2.39 (95% confidence interval 1.04–5.46, p = 0.04). The frequency of the SRD5A2 LL genotype in cases (29.3%) was also slightly higher than in controls (24.6%), but this was not significant. Regarding the A49T polymorphism of SRD5A2, we could not detect the T allele in any of the examined samples. These data suggest a significant association between the CYP17 polymorphism and prostate-cancer risk among the Japanese. © 2001 Wiley-Liss, Inc.

Published
2001
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6. Regulation of carcinoma cell invasion by protein C inhibitor whose expression is decreased in renal cell carcinoma.

Author

Wakita T, Hayashi T, Nishioka J, Tamaru H, Akita N, Asanuma K, Kamada H, Gabazza EC, Ido M, Kawamura J, and Suzuki K

Subjects
Adult, Aged, Aged, 80 and over, Carcinoma, Renal Cell metabolism, Cells, Cultured, Down-Regulation, Female, Hot Temperature, Humans, Kidney metabolism, Kidney pathology, Kidney Neoplasms metabolism, Male, Middle Aged, Neoplasm Invasiveness, Plasminogen Activator Inhibitor 1 genetics, Plasminogen Activator Inhibitor 1 metabolism, Promoter Regions, Genetic genetics, Protein C Inhibitor genetics, RNA, Messenger metabolism, Reverse Transcriptase Polymerase Chain Reaction, Serine Proteinase Inhibitors genetics, Transfection, Urokinase-Type Plasminogen Activator genetics, Urokinase-Type Plasminogen Activator metabolism, Carcinoma, Renal Cell pathology, Kidney Neoplasms pathology, Protein C Inhibitor metabolism, Serine Proteinase Inhibitors metabolism
Abstract

Protein C inhibitor (PCI), a member of the serine protease inhibitor family, is produced in various human tissues, including the liver, kidney and testis. In addition to inhibiting the anticoagulant protein C pathway, PCI also inhibits urinary plasminogen activator (uPA), which is a well-known mediator of tumor cell invasion. In the present study, to clarify the biologic significance of PCI in the kidney, we compared the expression of PCI between human renal cell carcinoma (RCC) tissue and nontumor kidney tissue. The PCI antigen level in RCC tissue was found to be significantly lower than in nontumor kidney tissue, and expression of PCI mRNA was detected in normal renal proximal tubular epithelial cells (RPTEC), but not in RCC or in an RCC cell line (Caki-1 cells). No differences were detected between the nucleotide sequence of the major cis-elements in the promoter region of the PCI gene from nontumor kidney and RCC tissues, RPTEC and Caki-1 cells, an RPTEC-derived RCC cell line. The in vitro invasiveness of Caki-1 cells transfected with a PCI expression vector was significantly decreased compared to mock-transfected Caki-1 cells, and it was blocked in the presence of anti-PCI antibody. Since PCI itself did not affect the proliferation rate of Caki-1 cells or cell expression of uPA in vitro, the effect of uPA, PCI, heat-inactivated PCI and plasminogen activator inhibitor (PAI)-1 on the invasive potential of cultured RCC cells was evaluated. The in vitro invasiveness of Caki-1 cells, which express uPA, was significantly enhanced by the addition of uPA, and it was inhibited by anti-uPA antibody, PCI and PAI-1, but not by heat-inactivated PCI. In addition, uPA activity was significantly decreased and uPA-PCI complex level was significantly increased in the culture medium of PCI expression vector-transfected Caki-1 cells as compared to mock-transfected Caki-1 cells. These findings strongly suggest that PCI regulates the invasive potential of RCC cells by inhibiting uPA secreted by these cells. The results of our study suggest that PCI might be a potential therapeutic agent for inhibiting renal tumor invasion., (Copyright 2003 Wiley-Liss, Inc.)

Published
2004
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