Protective actions of vitamin D in UVB induced skin cancer.

Protective actions of vitamin D in UVB induced skin cancer.
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DOI:
10.1039/c2pp25251a
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发表时间:
2012-12
期刊:
Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology
影响因子:
--
通讯作者:
Bikle DD
Bikle DD
中科院分区:
其他
文献类型:
--
作者:
Bikle DD

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非黑色素瘤皮肤癌(NMSC)是最常见的癌症类型,在美国每年发生超过100万例。虽然它们的转移潜力通常较低,但它们可以并且确实转移,特别是在免疫受损的宿主中,并且它们的手术治疗通常相当毁容。紫外线辐射(UVR)与阳光照射一起发生,通常被认为是这些恶性肿瘤的原因,但UVR也是皮肤中维生素D合成所必需的。根据我们自己的数据和文献报道,我们假设皮肤中产生的维生素D可以抑制UVR表皮肿瘤的形成。在这篇综述中,我们将首先讨论的证据支持的结论,维生素D受体(VDR),有或没有它的配体1,25-二羟维生素D,限制癌症形成的倾向以下UVR。然后,我们将探讨这种保护的三种潜在机制:抑制增殖和刺激分化,免疫调节和刺激DNA损伤修复(DDR)。
Non-melanoma skin cancers (NMSC) are the most common type of cancer, occurring at a rate of over 1 million per year in the United States. Although their metastatic potential is generally low, they can and do metastasize, especially in the immune compromised host, and their surgical treatment is often quite disfiguring. Ultraviolet radiation (UVR) as occurs with sunlight exposure is generally regarded as causal for these malignancies, but UVR is also required for vitamin D synthesis in the skin. Based on our own data and that reported in the literature, we hypothesize that the vitamin D produced in the skin serves to suppress UVR epidermal tumor formation. In this review we will first discuss the evidence supporting the conclusion that the vitamin D receptor (VDR), with or without its ligand 1,25-dihydroxyvitamin D, limits the propensity for cancer formation following UVR. We will then explore three potential mechanisms for this protection: inhibition of proliferation and stimulation of differentiation, immune regulation, and stimulation of DNA damage repair (DDR).
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