Anticancer activity of vitamin D – molecular mechanisms

A large number of studies have pointed to the relations between blood levels of 25-hydroxy vitamin D with cancer incidence and survival. The phenomenon of the multidirectional activity of vitamin D is possibly due to the presence of VDR in most nonskeletal human cells, including cancer cells. A wide range of the genes regulated by VDR are related with cell proliferation, apoptosis, differentiation, angiogenesis and metastasis. In some preclinical studies, colon, lung and BC have all demonstrated downregulation of VDR expression as compared to normal cells, and well-differentiated tumors have shown more VDR expression when compared to their poorly differentiated counterparts. Generally, higher tumor VDR expression has been noted as correlating with better prognosis in cancer patients. However, vitamin D pathway genetic polymorphisms also may influence cancer risk. VDR polymorphisms have received the most attention, but this influence has also been observed in genes related to vitamin D metabolism or signalling, such as: CYP27B1, CYP24A1, VDBP or RXRA. Even though the associations between most of them and cancers were not significant, some studies show that VDR polymorphisms may be a better or poor prognostic factor to assess the risk of cancer. The aim of this paper was to present the molecular pathways affected by vitamin D, which are included in carcinogenesis. The literature survey comprised of research compiled from mostly the last five years and it proves vitamin D as the most phenomenal among other vitamins.