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.