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Analysis of lymph node metastasis of oral cancer by using peroxiredoxin I knockout mouse

过氧化物酶I基因敲除小鼠口腔癌淋巴结转移分析

基本信息

批准号：
14370656
负责人：
YOSHIDA Hiroshi
金额：
$ 8.7万
依托单位：
University of Tsukuba
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2002
资助国家：
日本
起止时间：
2002 至 2004
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14370656/
关键词：
Peroxiredoxin knockout mouse gene trapping GATA-1 MSP23

项目摘要

Prx I deficient mouse was established by gene trapping method. Embryonic stem (ES) cells with a retroviral gene trap vector inserted into the Prx I locus (Omni bank no.OST422296) were transferred to a foster mother to generate chimeric animals (Lexicon Genetics Inc.). The genetic background was uniformized to C57BL/6 by back cross. B16 murine melanoma cells (1x10^5 cells/body) were inoculated into the mouse foot pad of three groups (wild-type, heterozygous, and homozygous Prx I deficient mouse) and lymph node metastasis and lung metastasis were observed. When genetic background was C57/129Sv, lymph node and lung metastasis were reduced by Prx I loss. However, after 5 generation back cross and uniformized C57BL/6 genetic background, there was no significant difference in lymph node and lung metastasis between wild-type and Prx I homozygous deficient mice. When another cell line (LLC cell, derived form lung cancer : 3x10^6 cells/body) was inoculated in these groups, there was no difference. By using Matrigel as a matrix of tumor growth, we inoculated the mixture of B16 cells (1x105 cells /body) and the gel into subcutaneous and investigated the vascularization, but there was no significant difference. On the other hand we investigated the stress response of A170 oxidative stress, which is regulated by same transcription factor Nrf2 as Prx I to analyze how oxidative stress protein was induce by oxidative stress. And we also investigated GATA-1 transgenic mouse, because Prx I and GATA-1 were both related with red blood cell abnormality.

采用基因捕获法建立Prx I缺陷小鼠模型。将具有插入Prx I基因座的逆转录病毒基因捕获载体的胚胎干（ES）细胞（Omni bank no. OST 422296）转移至寄养母体以产生嵌合动物（Lexicon Genetics Inc.）。通过回交将遗传背景统一到C57 BL/6。将B16鼠黑色素瘤细胞（1 × 10^5个细胞/个体）接种到三组（野生型、杂合型和纯合型Prx I缺陷小鼠）的小鼠足垫中，观察淋巴结转移和肺转移。当基因背景为C57/129 Sv时，Prx I缺失可减少淋巴结和肺转移。然而，经过5代回交和统一的C57 BL/6遗传背景，野生型和Prx I纯合缺陷小鼠之间的淋巴结和肺转移没有显著差异。当在这些组中接种另一种细胞系（LLC细胞，来源于肺癌：3x10^6个细胞/个体）时，没有差异。通过使用Matrigel作为肿瘤生长基质，我们将B16细胞（1x 105个细胞/体）和凝胶的混合物接种到皮下并观察血管化，但没有显着差异。另一方面，我们研究了A170细胞氧化应激的应激反应，该反应受与Prx I相同的转录因子Nrf 2调控，以分析氧化应激如何诱导氧化应激蛋白。由于Prx I和加塔-1都与红细胞异常有关，我们还对加塔-1转基因小鼠进行了研究。

项目成果

期刊论文数量（13）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Transgenic over-expression of GATA-1 mutant lacking N-finger domain causes hemolytic syndrome in mouse erythroid cells.

缺乏 N 指结构域的 GATA-1 突变体的转基因过度表达会导致小鼠红系细胞溶血综合征。

DOI：
发表时间：
2005
期刊：
Gene Cells 10
影响因子：
0
作者：
Nakano;M.;et al.
通讯作者：
et al.

Peroxiredoxin I expression in tongue squamous cell carcinomas as involved in tumor recurrence.

DOI：
10.1016/j.ijom.2005.04.015
发表时间：
2005-12
期刊：
International journal of oral and maxillofacial surgery
影响因子：
2.4
作者：
Toru Yanagawa;Ken Omura;Hiroyuki Harada;T. Ishii;Junya Uwayama;K. Nakaso;Satoshi Iwasa;Yumi Koyama;K. Onizawa;H. Yusa;Hiroshi Yoshida
通讯作者：
Toru Yanagawa;Ken Omura;Hiroyuki Harada;T. Ishii;Junya Uwayama;K. Nakaso;Satoshi Iwasa;Yumi Koyama;K. Onizawa;H. Yusa;Hiroshi Yoshida

Transgenic over-expression of GATA-1 mutant lacking N-finger domain causes hemolvtic syndrome in mouse erythroid cells

缺乏N指结构域的GATA-1突变体的转基因过度表达导致小鼠红系细胞溶血综合征