Background: Inhibition of human carcinomas has previously been linked to vitamin D due to its effects on cancer cell proliferation, migration, angiogenesis, and apoptosis induction. The anticancer activity of vitamin D has been confirmed by several studies, which have shown that increased cancer incidence is associated with decreased vitamin D and that dietary supplementation of vitamin D slows down the growth of xenografted tumors in mice. Vitamin D inhibits the growth of cancer cells by the induction of apoptosis as well as by arresting the cells at the G0/G1 (or) G2/M phase of the cell cycle. Aim and Key Scientific Concepts of the Review: The purpose of this article is to thoroughly review the existing information and discuss and debate to conclude whether vitamin D could be used as an agent to prevent/treat cancers. The existing empirical data have demonstrated that vitamin D can also work in the absence of vitamin D receptors (VDRs), indicating the presence of multiple mechanisms of action for this sunshine vitamin. Polymorphism in the VDR is known to play a key role in tumor cell metastasis and drug resistance. Although there is evidence that vitamin D has both therapeutic and cancer-preventive properties, numerous uncertainties and concerns regarding its use in cancer treatment still exist. These include (a) increased calcium levels in individuals receiving therapeutic doses of vitamin D to suppress the growth of cancer cells; (b) hyperglycemia induction in certain vitamin D-treated study participants; (c) a dearth of evidence showing preventive or therapeutic benefits of cancer in clinical trials; (d) very weak support from proof-of-principle studies; and (e) the inability of vitamin D alone to treat advanced cancers. Addressing these concerns, more potent and less toxic vitamin D analogs have been created, and these are presently undergoing clinical trial evaluation. To provide key information regarding the functions of vitamin D and VDRs, this review provided details of significant advancements in the functional analysis of vitamin D and its analogs and VDR polymorphisms associated with cancers.
背景：维生素D因其对癌细胞增殖、迁移、血管生成及凋亡诱导的作用，先前已被证实与抑制人类癌症相关。多项研究确认了维生素D的抗癌活性，表明癌症发病率升高与维生素D水平降低存在关联，且膳食补充维生素D可减缓小鼠异种移植肿瘤的生长。维生素D通过诱导细胞凋亡以及将细胞阻滞于细胞周期的G0/G1期或G2/M期来抑制癌细胞生长。综述目的与核心科学概念：本文旨在系统梳理现有研究资料，通过讨论与论证以明确维生素D是否可作为预防或治疗癌症的制剂。现有实证数据表明，维生素D在缺乏维生素D受体（VDR）的情况下仍能发挥作用，提示这种"阳光维生素"存在多重作用机制。已知VDR多态性在肿瘤细胞转移和耐药性中起关键作用。尽管有证据表明维生素D兼具治疗和预防癌症的特性，但其在癌症治疗中的应用仍存在诸多不确定性与争议，包括：（a）接受治疗剂量维生素D以抑制癌细胞生长的个体可能出现血钙水平升高；（b）部分维生素D治疗的研究参与者出现高血糖诱导现象；（c）临床试验中缺乏显示癌症预防或治疗获益的证据；（d）原理验证研究的支持力度薄弱；（e）单用维生素D无法治疗晚期癌症。针对这些问题，目前已研发出效力更强、毒性更低的维生素D类似物，并正在进行临床试验评估。为阐明维生素D及VDR功能的关键信息，本综述详细阐述了维生素D及其类似物的功能分析、以及与癌症相关的VDR多态性研究的重要进展。
肿瘤(癌症)患者之家