Shirley Stephanie H, Grimm Elizabeth A, Kusewitt Donna F
Department of Molecular Carcinogenesis, Science Park, The University of Texas MD Anderson Cancer Center, 1808 Park Road 1C, Smithville, TX 78957, USA.
J Skin Cancer. 2012;2012:410925. doi: 10.1155/2012/410925. Epub 2012 Jun 13.
Despite extensive investigation, the precise contribution of the ultraviolet radiation (UVR) component of sunlight to melanoma etiology remains unclear. UVR induces keratinocytes to secrete proinflammatory and immunomodulatory mediators that promote inflammation and skin tumor development; expression of the slug transcription factor in keratinocytes is required for maximal production of these mediators. In the present studies we examined the possibility that UVR-exposed melanocytes also produce proinflammatory mediators and that Slug is important in this process. Microarray studies revealed that both UVR exposure and Slug overexpression altered transcription of a variety of proinflammatory mediators by normal human melanocytes; some of these mediators are also known to stimulate melanocyte growth and migration. There was little overlap in the spectra of cytokines produced by the two stimuli. However IL-20 was similarly induced by both stimuli and the NFκB pathway appeared to be important in both circumstances. Further exploration of UVR-induced and Slug-dependent pathways of cytokine induction in melanocytes may reveal novel targets for melanoma therapy.
尽管进行了广泛的研究,但阳光中的紫外线辐射(UVR)成分对黑色素瘤病因的确切作用仍不清楚。UVR诱导角质形成细胞分泌促炎和免疫调节介质,促进炎症和皮肤肿瘤发展;角质形成细胞中蛞蝓转录因子的表达是这些介质最大量产生所必需的。在本研究中,我们研究了暴露于UVR的黑素细胞是否也产生促炎介质以及蛞蝓在这一过程中是否重要。微阵列研究表明,UVR暴露和蛞蝓过表达均改变了正常人黑素细胞中多种促炎介质的转录;其中一些介质也已知可刺激黑素细胞生长和迁移。两种刺激产生的细胞因子谱几乎没有重叠。然而,IL-20在两种刺激下均被类似诱导,并且NFκB途径在两种情况下似乎都很重要。进一步探索黑素细胞中UVR诱导的和蛞蝓依赖性细胞因子诱导途径可能会揭示黑色素瘤治疗的新靶点。