| [ Summary ] |
Active vitamin D has been shown to exert antitumor effects by causing G1 arrest, and inducing differentiation and apoptosis of a wide variety of malignant cells, after binding to VDR. However, target molecules of VDR and its mechanisms of action remain unclear. VDR knockout mice and cells should provide a valuable model for unraveling the genetic link between VDR and pathogenetic pathways to carcinogenesis (apoptosis resistance to radiation and chemotherapeutics, cell cycle checkpoint dysregualtion including G1arrest, de-differentiation etc.). |