Vitamin D for the prevention and treatment of pancreatic cancer

Figure 1 Mechanisms of Vitamin D₃ action on pancreas cells. Both 1,25(OH)₂D₃ and 25(OH)D₃ can enter pancreas cells, where 25(OH)D₃ can be converted to 1,25(OH)₂D₃ by 1α-OHase. 1,25(OH)₂D₃ can bind the VDR and further combine with the retinoid X receptor (RXR) to form a heterodimer, VDR-RXR. The VDR-RXR heterodimer binds to specific vitamin D response elements located in the promoter region of vitamin D-responsive genes, which in turn induces gene transcription. So far, in terms of pancreas cells, inhibition of CDK2, CDK4, Cyclin D1, Cyclin E, Cyclin A and upregulation of p21 and p27 have been demonstrated, leading to a block in the cell cycle at G0/G1. Regarding induction of differentiation, apoptosis and other anticancer mechanisms, further studies are required.