Irradiation of cells with ultraviolet light (UV) leads to modifications of c‐Jun resembling those elicited by phorbol esters or oncogenes, and to enhanced transcription of AP‐1‐dependent genes. The UV‐induced signal also triggers activation of Raf‐1 and MAP‐2 kinases. A dominant‐negative Raf‐1 kinase mutant strongly interferes with both phorbol ester and UV‐induced AP‐1 activation, indicating obligatory involvement of identical components in cytoplasmic signal transduction. Thus, from a presumably nuclear site of energy absorption, a signal needs to be transmitted to the cytoplasm in order to achieve activation of a nuclear transcription factor. Further, signals elicited from different primary sites merge prior to or at the level of activation of Raf‐1 kinase.
Transfection of a cloned p53 gene into a murine bladder carcinoma cell with a low metastatic capacity led to elevated levels of p53 protein in clonal transfectants. After intravenous inoculation into syngeneic mice, p53-transfected clones showed significantly increased metastatic potential in comparison with control transfectants. The observed change did not seem to be due to a change in growth potential per se since the cell lines showed similar growth properties in vitro.
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