Abstract
Solar ultraviolet (UV) radiation is an important environmental factor that leads to immune suppression, inflammation, photoaging, and skin carcinogenesis. Here, we reviewed the specific signal transduction pathways and transcription factors involved in the cellular response to UV-irradiation. Increasing experimental data supporting a role for p38, MAPK, JNK, ERK1/2, and ATM kinases in the response network to UV exposure is discussed. We also reviewed the participation of NF-κB, AP-1, and NRF2 transcription factors in the control of gene expression after UV-irradiation. In addition, we discussed the promising chemotherapeutic intervention of transcription factors signaling by natural compounds. Finally, we focused on the review of data emerging from the use of DNA microarray technology to determine changes in global gene expression in keratinocytes and melanocytes in response to UV treatment. Efforts to obtain a comprehensive portrait of the transcriptional events regulating photodamage of intact human epidermis after UV exposure reveals the existence of novel factors participating in UV-induced cell death. Progress in understanding the multitude of mechanisms induced by UV-irradiation could lead to the potential use of protein kinases and novel proteins as specific targets for the prevention and control of skin cancer.
Highlights
Ultraviolet radiation from sunlight is an environmental factor that has a variety of physiological and biological effects, including immune suppression, cellular aging, DNA damage and initiation of apoptosis [1,2]
mitogen-activated protein kinases (MAPKs) and phosphatidylinositol 3-kinase (PI-3K) pathways can regulate each other in response to UV radiation; extracellular signal-regulated kinase (ERK), p38K and c-Jun NH2-Terminal Kinases (JNK) activate specific transcription factors, which regulate the expression of genes participating in proliferation or cell survival
The MAPK signaling pathways are, in general, subdivided into three different pathways, namely the extracellular signal-regulated kinases (ERK), p38 MAPK (p38 kinase), and c-Jun NH2-terminal kinases (JNK) signaling pathways [29], which are activated by dual phosphorylation of threonine and tyrosine, at TX-Y motifs within their activation loops
Summary
Ultraviolet radiation from sunlight is an environmental factor that has a variety of physiological and biological effects, including immune suppression, cellular aging, DNA damage and initiation of apoptosis [1,2]. UV-A and UV-B portion has a strong carcinogenic effect on the skin [9,10,11] to directly or indirectly induce DNA damage leading to genomic mutations and modified gene expression [8,12,13]. In addition to DNA damage, UV enhances the production of reactive oxygen species (ROS) and induces activation of specific signal transduction pathways, resulting in altered gene expression that induce senescence, cell cycle arrest and cell death [16,17,18]
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