Ronai Z A, Okin E, Weinstein I B
Comprehensive Cancer Center, Columbia University, New York, NY 10032.
Oncogene. 1988 Feb;2(2):201-4.
The exposure of a polyoma virus transformed rat fibroblast cell line H3 to UV-C irradiation (254 nm) causes a transient increase in the abundance of RNAs for the cellular oncogenes c-H-ras, c-myc and c-fos, as well as RNAs homologous to an endogenous rat leukemia virus-related sequence (RaLV). Treatment with cycloheximide also causes a transient increase in the c-H-ras, c-myc and RaLV RNAs, with a time course similar to that obtained with UV irradiation. UV-C irradiation also causes a transient increase in the RNAs for c-H-ras and c-myc in an SV40 transformed human keratinocyte cell line SVK-14. Dose response studies with UV light at the various wavelengths found in sunlight indicate that UV-B (270-330 nm) and UV-A (345-440 nm) are much less potent than UV-C in inducing increased levels of c-H-ras and c-myc RNAs in SVK-14 cells. Thus, in addition to the well known mutagenic effects of UV irradiation, UV damage to DNA can also lead to increased expression of cellular oncogenes in both rodent fibroblasts and human keratinocytes.
将多瘤病毒转化的大鼠成纤维细胞系H3暴露于UV-C辐射（254 nm）会导致细胞癌基因c-H-ras、c-myc和c-fos的RNA丰度短暂增加，以及与内源性大鼠白血病病毒相关序列（RaLV）同源的RNA丰度短暂增加。用环己酰亚胺处理也会导致c-H-ras、c-myc和RaLV RNA短暂增加，其时间进程与UV照射相似。UV-C辐射还会使SV40转化的人角质形成细胞系SVK-14中c-H-ras和c-myc的RNA短暂增加。对阳光中发现的各种波长的紫外线进行剂量反应研究表明，UV-B（270 - 330 nm）和UV-A（345 - 440 nm）在诱导SVK-14细胞中c-H-ras和c-myc RNA水平升高方面的效力远低于UV-C。因此，除了紫外线辐射众所周知的诱变作用外，紫外线对DNA的损伤还可导致啮齿动物成纤维细胞和人角质形成细胞中细胞癌基因的表达增加。
