权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Role of metallothionein on carcinogenesis and tumor progression in bladder cancer.

金属硫蛋白在膀胱癌发生和肿瘤进展中的作用。

基本信息

批准号：
11671586
负责人：
KONDO Yukihiro
金额：
$ 2.3万
依托单位：
Nippon Medical School
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2000
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11671586/
关键词：
bladder cancer metallothionein carcinogenesis tumor progression 増殖因子亜鉛 BBN

项目摘要

(1) Immortalized metallothionein null cellsImmortalized metallothionein(MT) null cells were established by transfection of simian virus 40 into MT null fibroblast. Additionally, immortalized control fibroblast were established. Immortalized MT null cells showed increased sensitivity cadmium not to zinc, copper, mercury or nickel. These results were written in Life Science, 64,1999,145-150.(2) Metallothionein prevents the carcinogenicity.We examined the carcinogenicity of N-butyl-N-(4-hydroxybutyl) nitrosamine(BBN) in transgenic mice deficient in the MT I and II genes and control (129/Sv) mice. BBN induced bladder tumors in 75% of MT null mice and in 43% of 129/Sv mice. The average number of bladder tumors per mouse was significantly higher in MT null mice than in 129/Sv mice. Zinc treatment suppressed the carcinogenicity of BBN in 129/Sv mice but not in MT null mice. These results were written in Carcinogenesis, 20, 1999, 1625-1627.(3) Histopathologic examinationHistopathologic examination revealed that all tumor samples showed morphological changes characteristic of transitional cell carcinoma in both MT null and 129/Sv mice. The major bladder tumors in 129/Sv mice displayed the features of high grade, whereas none of the tumors in MT null mice were designated as grade III.Thus, the malignant potential of bladder tumors in 129/Sv mice was greater than that in MT null mice.(4) MT null bladder tumor cell lineWe established MT null and 129/Sv bladder tumor cell line. MT null bladder tumor cells were unable to induced MT by administered cadmium. These cells were sensitive to cadmium and cisplatin against 129/Sv bladder tumor cells.

(1)金属硫蛋白灭活细胞通过将猴病毒40转染到金属硫蛋白灭活成纤维细胞中，建立金属硫蛋白灭活细胞。此外，还建立了永生化对照成纤维细胞。永生化MT零细胞对镉的敏感性增加，而对锌、铜、汞或镍的敏感性增加。这些研究结果发表在《生命科学》1999年第64期，145-150页。(2)金属硫蛋白防止致癌性。我们检测了n -丁基- n -（4-羟基丁基）亚硝胺（BBN）在缺乏MT I和II基因的转基因小鼠和对照（129/Sv）小鼠中的致癌性。BBN在75%的MT阴性小鼠和43%的129/Sv小鼠中诱发膀胱肿瘤。MT阴性小鼠平均每只小鼠膀胱肿瘤数明显高于129/Sv小鼠。锌处理在129/Sv小鼠中抑制BBN的致癌性，而在MT无效小鼠中没有。这些结果发表在癌变，1999,20,1625-1627。(3)组织病理学检查：MT null和129/Sv小鼠的所有肿瘤标本均表现出移行细胞癌的形态学变化特征。129/Sv小鼠的主要膀胱肿瘤表现为高分级特征，而MT null小鼠的肿瘤均未被定为III级。因此，129/Sv小鼠膀胱肿瘤的恶性潜能大于MT阴性小鼠。(4) MT null膀胱肿瘤细胞系我们建立了MT null和129/Sv膀胱肿瘤细胞系。MT空膀胱肿瘤细胞不能被镉诱导MT。这些细胞对镉和顺铂对129/Sv膀胱肿瘤细胞敏感。