Rescue of cells from ras oncogene-induced growth arrest by a second, complementing, oncogene.
Rescue of cells from ras oncogene-induced growth arrest by a second, complementing, oncogene.
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DOI：
10.1073/pnas.85.5.1519
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发表时间：
1988-03
影响因子：
11.1
通讯作者：
T. Hirakawa;H. Ruley
中科院分区：
文献类型：
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作者：
T. Hirakawa;H. Ruley
建立的REF 52细胞（大鼠胚胎成纤维细胞）完全抵抗ras癌基因的稳定转化，猴病毒40大肿瘤（T）抗原与ras合作将REF 52细胞转化为致瘤状态。温度敏感的猿猴病毒40大T抗原（由tsA 58编码）允许T24 Ha-ras癌基因以温度依赖性方式转化REF 52细胞。三分之二的克隆转化tsA 58和ras成为停滞在G2期或后期S期时，转移到一个nonpermissive温度T抗原的稳定性。因此，ras诱导生长停滞，而不是稳定的转化，在没有一个功能性的合作癌基因。这些结果表明，合作的癌基因可以调节细胞对ras的反应，并对控制表达激活的ras癌基因的肿瘤细胞的治疗策略有影响。
Established REF52 cells (rat embryo fibroblasts) completely resist stable transformation by ras oncogenes, and simian virus 40 large tumor (T) antigen collaborates with ras to convert REF52 cells to tumorigenic state. A temperature-sensitive simian virus 40 large T antigen (encoded by tsA58) allowed the T24 Ha-ras oncogene to transform REF52 cells in a temperature-dependent manner. Two thirds of the clones transformed with tsA58 and ras became arrested in G2 or late S phase when shifted to a nonpermissive temperature for T antigen stability. Thus, ras induced growth arrest rather than stable transformation in the absence of a functional collaborating oncogene. These results indicate that collaborating oncogenes can regulate cellular responses to ras and have implications regarding therapeutic strategies to control tumor cells expressing activated ras oncogenes.