Resistance to Oncogenic Transformation in Revertant R1 of Human ras-Transformed NIH 3T3 cells

Kuzumaki, Noboru; Ogiso, Yoshifumi; Oda, Atsushi et al.

Molecular and Cellular Biology, 1989, 9(5), 2258-2263

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アクセス権
open access
URI
https://hdl.handle.net/2115/753
タイトル
Resistance to Oncogenic Transformation in Revertant R1 of Human ras-Transformed NIH 3T3 cells
著者
Kuzumaki, Noboru ; Ogiso, Yoshifumi ; Oda, Atsushi ; Fujita, Hisakazu ; Suzuki, Hiroaki ; Sato, Chiharu ; Mullauer, Leonhard
著者名
Kuzumaki, Noboru
葛巻, 暹
著者名
Ogiso, Yoshifumi
著者名
Oda, Atsushi
著者名
Fujita, Hisakazu
著者名
Suzuki, Hiroaki
著者名
Sato, Chiharu
著者名
Mullauer, Leonhard
言語
英語
発行日
1989
出版者
American Society for Microbiology
収録物名
Molecular and Cellular Biology
巻(号)
9(5)
ページ
2258-2263
抄録
A flat revertant, R1, was isolated from human activated c-Ha-ras-1 (hu-ac-Ha-ras) gene-transformed NIH 3T3 cells (EJ-NIH 3T3) treated with mutagens. R1 contained unchanged transfected hu-ac-Ha-ras DNA and expressed high levels of hu-ac-Ha-ras-specific mRNA and p21 protein. Transfection experiments revealed that NIH 3T3 cells could be transformed by DNA from R1 cells but R1 cells could not be retransformed by Kirsten sarcoma virus, DNA from EJ-NIH 3T3 cells, hu-ac-Ha-ras, v-src, v-mos, simian virus 40 large T antigen, or polyomavirus middle T antigen. Somatic cell hybridization studies showed that R1 was not retransformed by fusion with NIH 3T3 cells and suppressed anchorage independence of EJ-NIH 3T3 and hu-ac-Ha-ras gene-transformed rat W31 cells in soft agar. These results suggest that the reversion and resistance to several oncogenes in R1 is due not to cellular defects in the production of the transformed phenotype but rather to enhancement of cellular mechanisms that suppress oncogenic transformation.
資源タイプ
学術雑誌論文
出版タイプ
Accepted Manuscript
権利情報
Copyright (c) 1989 American Society for Microbiology
PISSN
02707306