Vitamin D Treatment Tames Colon Cancer Cells

They treated the growing cells with calcitriol (1,25-dihydroxyvitamin D3), the metabolically active form of vitamin D.
Results published in the November 17, 2008, issue of the Journal of Cell Biology, revealed that calcitriol treatment triggered a chain of metabolic events beginning with the activation of the vitamin D receptor (VDR), a transcription factor of the nuclear receptor superfamily. Binding of cacitriol to VDR induced a transcription-independent calcium influx and activation of RhoA–Rho-associated coiled kinase (ROCK). This step was followed by activation of the p38 mitogen-activated protein kinase (p38MAPK) and mitogen- and stress-activated kinase 1 (MSK1). RhoA–ROCK and MSK1 were also required for the inhibition of Wnt–beta-catenin pathway and cell proliferation.

The end result was inhibition of cell division and remodeling of colon cancer cells into epithelial cells. These finds help clarify the actions of a molecule that is currently undergoing clinical trials as a cancer therapy.

Related Links:
Científicas-Universidad Autónoma