VITAMIN D3 AND CANCER PREVENTION: FROM BIOLOGICAL MECHANISM TO CLINICAL EVIDENCE

Vitamin D3 (cholecalciferol) is a steroid prohormone synthesized in the skin as a result of UV-B light exposure or by dietary intake. In addition to the already proven action on calcium phosphate metabolism and bone physiology, there is an increasing body of research showing that vitamin D3 may impact carcinogenesis and cancer progression. The aim of this literature review was to summarize current knowledge regarding the biological mechanisms of vitamin D₃ and its potential impact on cancer risk, progression, and patient survival. Multiple observational trials have confirmed that there is an inverse relationship between levels of serum 25-hydroxyvitamin D [25(OH)D] and the risk as well as mortality rates associated with some types of cancer, especially colorectal and breast cancers. However, findings from randomized controlled trials evaluating primary cancer prevention remain inconclusive. Such contradicting findings have been linked to limitations in research design, which include insufficient supplementation doses, inclusion of participants with adequate baseline vitamin D status, and relatively short follow-up periods. Vitamin D exerts its action via the vitamin D receptor (VDR) at the molecular level. It affects the gene expression related to various functions such as the cell cycle, apoptosis, cellular differentiation, immune modulation, and inflammatory processes. Current scientific evidence supports a mechanism by which vitamin D3 could play a part in the prevention of cancer. However, clear clinical recommendations require further well-designed randomized controlled trials incorporating adequate supplementation doses and focusing on populations with vitamin D deficiency.