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首页> 外文期刊>Seminars in cancer biology >UVA-mediated activation of signaling pathways involved in skin tumor promotion and progression.
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UVA-mediated activation of signaling pathways involved in skin tumor promotion and progression.

机译：UVA介导的涉及皮肤肿瘤促进和进展的信号传导途径的激活。

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Each year more than 1,000,000 cases of non-melanoma skin cancer (NMSC) are diagnosed in the Unites States. Solar radiation has been described as an important etiological factor in the development of NMSC. UVA comprises the largest portion of solar radiation reaching the surface of the earth (90-99%) and has been described to lead to benign tumor formation as well as malignant cancers, squamous cell carcinomas (SCCs). While much research has focused upon the effects of UVB radiation, little is known about UVA-induced signaling pathways and their role in tumor promotion. Here we focus on UVA-mediated activation of mitogen-activated protein kinase (MAPK) pathways and their role in activator protein-1 (AP-1) mediated transcription and cyclooxygenase-2 (COX-2) expression. AP-1 and COX-2 have been found to play a role in angiogenesis in other tissues. We propose UVA-mediated increases in AP-1 and COX-2 may play a role in tumor promotion through increases in interleukin-8 (IL-8) and vascular endothelial growth factor (VEGF). Since MAPKs, specifically p38 and JNK, appear to play a major role in the expression of UVA-induced AP-1 and COX-2, pharmacological inhibitors may be of benefit in the chemoprevention of non-melanoma skin cancer.
机译：每年在美国诊断出超过1,000,000例非黑色素瘤皮肤癌（NMSC）病例。太阳辐射已被描述为NMSC发展的重要病因。 UVA包括到达地球表面的太阳辐射的最大部分（占90-99％），并且已被描述为导致良性肿瘤形成以及恶性癌，鳞状细胞癌（SCC）。尽管许多研究都集中在UVB辐射的影响上，但对UVA诱导的信号通路及其在肿瘤促进中的作用知之甚少。在这里，我们专注于UVA介导的丝裂原活化蛋白激酶（MAPK）途径的激活及其在激活蛋白1（AP-1）介导的转录和环氧合酶2（COX-2）表达中的作用。已经发现AP-1和COX-2在其他组织的血管生成中起作用。我们建议UVA介导的AP-1和COX-2的增加可能通过白介素8（IL-8）和血管内皮生长因子（VEGF）的增加在肿瘤促进中发挥作用。由于MAPK，特别是p38和JNK，似乎在UVA诱导的AP-1和COX-2的表达中起主要作用，因此药理抑制剂可能在非黑素瘤皮肤癌的化学预防中受益。

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