The pivotal role of vitamin D, specifically its receptor (VDR), in slowing down the action of a key protein in the carcinogenic transformation process of colon cancer cells has been confirmed in a new study.
Researchers at the Vall d'Hebron Institute of Oncology (VHIO) collaborated with the Alberto Sols Institute of Biomedical Research (CSIC-UAB) for the study.
This protein, known as beta-catenin, which is normally found in intestinal epithelial cells where it facilitates their cohesion, builds up in large quantities in other areas of the cells when the tumour transformation begins.
As a result of these changes, the protein is retained in the cell nucleus, where it facilitate the carcinogenic process, and this is the point at which vitamin D intervenes, or rather, the vitamin D receptor (VDR).
"Our study has confirmed the pivotal role of the VDR in controlling the anomalous signal that sparks off the growth and uncontrolled proliferation of colon cells which, in the final instance, ends up causing a tumour to emerge," said Hector Palmer, the coordinator of the study and head of the VHIO's Stem Cells and Cancer laboratory.
"The stimulation of this receptor suppresses the action of the beta-catenin protein, intercepting the series of events that change the intestinal cell into a malignant tumour cell," he added.
The researchers analysed the effect of the VDR on human colon cancer cell cultures and observed that the concentration of the altered protein, beta-catenin, increased in cells without the VDR.
In light of these findings, chronic vitamin D deficiency represents a risk factor in the development of more aggressive colon tumours.
These results were being published in the journal PLoS One.