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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Vitamin D receptor, a tumor suppressor in skin
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Vitamin D receptor, a tumor suppressor in skin

机译：维生素D受体，皮肤中的肿瘤抑制因子

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Vitamin D and calcium are well-established regulators of keratinocyte proliferation and differentiation. Therefore, it was not a great surprise that deletion of the vitamin D receptor (VDR) should predispose the skin to tumor formation, and that the combination of deleting both the VDR and calcium sensing receptor (CaSR) should be especially pro-oncogenic. In this review I have examined 4 mechanisms that appear to underlie the means by which VDR acts as a tumor suppressor in skin. First, DNA damage repair is curtailed in the absence of the VDR, allowing mutations in DNA to accumulate. Second and third involve the increased activation of the hedgehog and beta-catenin pathways in the epidermis in the absence of the VDR, leading to poorly regulated proliferation with reduced differentiation. Finally, VDR deletion leads to a shift in the expression of long noncoding RNAs toward a more oncogenic profile. How these different mechanisms interact and their relative importance in the predisposition of the VDR null epidermis to tumor formation remain under active investigation.
机译：维生素D和钙是公认的角质形成细胞增殖和分化调节剂。因此，维生素D受体（VDR）的缺失应使皮肤易于形成肿瘤，并且VDR和钙敏感受体（CaSR）的缺失相结合尤其具有促癌性，这并不令人感到意外。在这篇综述中，我研究了4种机制，这些机制似乎是VDR充当皮肤肿瘤抑制剂的手段的基础。首先，在没有VDR的情况下减少了DNA损伤修复，使DNA突变得以积累。第二个和第三个涉及在没有VDR的情况下表皮中刺猬和β-catenin途径的激活增加，导致增殖调控不佳，分化降低。最后，VDR缺失导致长非编码RNA的表达向致癌性更强的方向转移。这些不同的机制如何相互作用以及它们在VDR空表皮对肿瘤形成的易感性中的相对重要性仍在积极研究中。

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