Elliott G C, Johnson R T
Mutat Res. 1985 May;145(3):185-94. doi: 10.1016/0167-8817(85)90026-4.
Ultraviolet light-induced excision repair, as measured by single-strand DNA-break accumulation in the presence of hydroxyurea and 1-beta-D-arabinofuranosylcytosine, undergoes an apparent decline concomitant with spontaneous transformation of mouse cells in vitro. This decline is seen in preneoplastic transformed cells as well as tumorigenic cells, suggesting that it is an early event in transformation. The difference between nontransformed and transformed mouse cells in apparent incision rates is greatest at short times after irradiation when nontransformed cells show a transient phase of rapid incision. No gross differences in the effects of UV on replicative DNA synthesis, bulk RNA synthesis, cell proliferation or clonal survival in nontransformed and transformed cells were seen, in spite of the reduced incision capacity of the latter. Taken together the results suggest that transformed cells are capable of growth in the presence of significantly increased amounts of DNA damage. A decreased ability of nontumorigenic cells to remove DNA lesions, coupled with unrestricted growth, may be responsible for genetic alterations which increase the probability of a cell becoming tumorigenic.
通过在羟基脲和1-β-D-阿拉伯呋喃糖基胞嘧啶存在下单链DNA断裂积累来测定的紫外线诱导切除修复，在体外小鼠细胞自发转化的同时明显下降。这种下降在癌前转化细胞以及致瘤细胞中均可见，表明这是转化过程中的早期事件。未转化和转化的小鼠细胞在明显切口率上的差异在照射后短时间内最大，此时未转化细胞表现出快速切口的短暂阶段。尽管转化细胞的切口能力降低，但在未转化和转化细胞中，紫外线对复制性DNA合成、大量RNA合成、细胞增殖或克隆存活的影响没有明显差异。综合这些结果表明，转化细胞能够在DNA损伤量显著增加的情况下生长。非致瘤细胞去除DNA损伤的能力下降，再加上不受限制的生长，可能是导致遗传改变的原因，而这种改变增加了细胞变成致瘤细胞的可能性。
