Noda M, Kitayama H, Matsuzaki T, Sugimoto Y, Okayama H, Bassin R H, Ikawa Y
Laboratory of Molecular Oncology, Tsukuba Life Science Center, Institute of Physical and Chemical Research, Ibaraki, Japan.
Proc Natl Acad Sci U S A. 1989 Jan;86(1):162-6. doi: 10.1073/pnas.86.1.162.
Seven morphologically nontransformed (flat) revertants with reduced tumorigenicity in vivo have been isolated from populations of Kirsten sarcoma virus-transformed NIH 3T3 cells transfected with a cDNA expression library of normal human fibroblasts. Each revertant harbors 1-10 recombinant plasmids per cell and retains a rescuable transforming virus as well as high level expression of v-Ki-ras-specific RNA and the viral oncogene product, p21v-Ki-ras. Transformed phenotypes are suppressed in cell hybrids generated by fusing each revertant to v-Ki-ras-transformed NIH 3T3 cells. From two of the revertant lines, plasmids capable of giving rise to flat secondary transfectants have been recovered. Thus, in some, if not all, of the revertants, transfected cDNAs seem to be responsible for the suppression of specific transformed phenotypes.
从用正常人成纤维细胞cDNA表达文库转染的 Kirsten 肉瘤病毒转化的 NIH 3T3 细胞群体中，分离出了七个在体内致瘤性降低的形态学上未转化（扁平）的回复突变体。每个回复突变体每个细胞含有1-10个重组质粒，并保留一种可拯救的转化病毒以及v-Ki-ras特异性RNA和病毒癌基因产物p21v-Ki-ras的高水平表达。通过将每个回复突变体与v-Ki-ras转化的 NIH 3T3 细胞融合产生的细胞杂种中，转化表型受到抑制。从两个回复突变体系中，回收了能够产生扁平二级转染子的质粒。因此，在一些（如果不是全部）回复突变体中，转染的cDNA似乎是特定转化表型抑制的原因。
