Abstract
Exposure to sunlight is the major cause of skin cancer. Ultraviolet radiation (UV) from the sun causes damage to DNA by direct absorption and can cause skin cell death. UV also causes production of reactive oxygen species that may interact with DNA to indirectly cause oxidative DNA damage. UV increases accumulation of p53 in skin cells, which upregulates repair genes but promotes death of irreparably damaged cells. A benefit of sunlight is vitamin D, which is formed following exposure of 7-dehydrocholesterol in skin cells to UV. The relatively inert vitamin D is metabolized to various biologically active compounds, including 1,25-dihydroxyvitamin D3. Therapeutic use of vitamin D compounds has proven beneficial in several cancer types, but more recently these compounds have been shown to prevent UV-induced cell death and DNA damage in human skin cells. Here, we discuss the effects of vitamin D compounds in skin cells that have been exposed to UV. Specifically, we examine the various signaling pathways involved in the vitamin D-induced protection of skin cells from UV.
Highlights
Ultraviolet radiation (UV) from the sun is well known to cause skin cell damage that leads to melanoma and non-melanoma skin cancer
Treatment with 1,25D inhibited the activation of stress-activated protein kinases, c-Jun N-terminal kinase (JNK), which lead to apoptosis in UV irradiated keratinocytes [26], and inhibited apoptosis induced by oxidative stress, TNFα and hydrogen peroxide cytotoxicity [25,63,64], possibly by increasing inherent antioxidant systems
The mitogen activated protein kinase (MAPK) cascade is a large group of conserved protein serine/threonine kinases which consist of three distinct tiers of protein kinases; a mitogen-activated extracellular signal-regulated kinase kinase kinase (MEKK), which activates a mitogen-activated extracellular signal-regulated kinase kinase (MEK) that subsequently activates a MAPK
Summary
Ultraviolet radiation (UV) from the sun is well known to cause skin cell damage that leads to melanoma and non-melanoma skin cancer. Exposure of 7-dehydrocholesterol in skin cells to UVB leads to production of pre-vitamin. The potentially harmful effects of UV radiation on skin cells include DNA damage and the production of reactive oxygen species (ROS) that interact with DNA and other molecules causing oxidative damage [6]. DNA damage and signal transduction pathways that are activated in response to stress related protein kinases activate a DNA damage response that leads to cell cycle arrest. This permits removal of DNA lesions by DNA repair enzymes before transcription and replication, or removal of irreparably damaged cells by apoptosis [1,17]. DNA damage and imbalances in antioxidant enzyme systems and scavengers are factors responsible for the induction of pro-apoptotic signaling pathways that lead to cell death
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