| Project/Area Number |
04671008
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
IMAMURA Toshiro Medical Institute of Bioregulation Kyushu Univ.Lecturer, 生体防御医学研究所, 助手 (10221095)
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| Co-Investigator(Kenkyū-buntansha) |
WAKE Norio Medical Institute of Bioregulation Kyushu Univ.Professor, 生体防御医学研究所, 教授 (50158606)
加藤 秀則 九州大学, 生体防御医学研究所, 助手 (60214392)
宮本 新吾 九州大学, 生体防御医学研究所, 助手 (40209945)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1993: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1992: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Human endometraial carcinoma / Human chromosome 1 / cDNA expression vector library / Actin stress fibers / Tumor suppressor gene / cDNAライブラリー / 微小核融合 / 染色体 |
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| Research Abstract |
We previously showed that introduction of a single human chromosome 1,6, or 9 derived from normal fibroblasts into HHUA endometrial carcinoma cells resulted in suppression of tumorigenicity. The tumorigenic suppression was accompanied by remarkable morphological changes in the microcell hybrids containing an extra copy of chromosome 1. The study presented here was undertaken to search for target cytoskeletal components affected by chromosome 1 transfer into endometrial carcinoma cells. We found that the microcell hybrids containing an extra copy of chromosome 1 were characterized by intracellulaactin bundle formation and an excessive accumulation of actin and vinculin. The latter was a result of increased stabilization of the proteins. Additionally, chromosome 3 introduction into RCC23 human renal carcinoma cells resulted in prolongation of cell division and in senescence of the significant proportion of the microcell hybrids. In thses microcell hybrids, the intracellular actin network was also reorganized, but the amounts of actin and vinculin protein were not increased. These findings suggest that increased actin organization, which appeared not to cause tumorigenic suppression in the microcell hybrids, is associated with complementation of tumor suppressor genes and senescence by multiple mechanisms.
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