Dhanwada K R, Dickens M, Neades R, Davis R, Pelling J C
Eppley Cancer Research Institute, University of Nebraska Medical Center, Omaha, USA.
Oncogene. 1995 Nov 16;11(10):1947-53.
Exposure to solar ultraviolet (UV) light is a major cause of skin cancer, the most common human neoplasm. The earth's upper atmosphere absorbs the high energy UV-C wavelengths (100-280 nm), while allowing transmission of UV-B (280-320 nm) and UV-A (320-400 nm). It is therefore UV-B and to some extent UV-A, that contributes to most human skin malignancies. We report that the exposure of cultured keratinocytes or skin to UV-C radiation causes activation of MAP kinases (ERK and JNK). In contrast, the solar radiation associated with skin cancer (UV-B) was an ineffective activator of the ERK and JNK signal transduction pathways. Therefore, while exposure of epidermal cells to UV-C radiation under laboratory conditions causes marked activation of MAP kinase signal transduction pathways, only a low level of MAP kinase signaling is involved in the response of skin to biologically relevant solar radiation.
暴露于太阳紫外线（UV）是皮肤癌的主要病因，皮肤癌是人类最常见的肿瘤。地球的上层大气吸收高能紫外线C波长（100 - 280纳米），同时允许紫外线B（280 - 320纳米）和紫外线A（320 - 400纳米）透过。因此，紫外线B以及在一定程度上紫外线A，是导致大多数人类皮肤恶性肿瘤的原因。我们报告，培养的角质形成细胞或皮肤暴露于紫外线C辐射会导致丝裂原活化蛋白激酶（ERK和JNK）的激活。相比之下，与皮肤癌相关的太阳辐射（紫外线B）对ERK和JNK信号转导途径的激活无效。因此，虽然在实验室条件下表皮细胞暴露于紫外线C辐射会导致丝裂原活化蛋白激酶信号转导途径的显著激活，但只有低水平的丝裂原活化蛋白激酶信号传导参与皮肤对具有生物学相关性的太阳辐射的反应。
