A study conducted by VHIO researchers confirms that a lack of vitamin D increases the aggressiveness of colon cancer.
The indication that vitamin D and its derivatives have a protective effect against various types of cancer is not new. In the field of colon cancer, numerous experimental and epidemiological studies show that vitamin D3 (or cholecalciferol) and some of its derivatives inhibit the growth of cancerous cells. Researchers at the Vall d'Hebron Institute of Oncology (VHIO), in collaboration with the Alberto Sols Institute of Biomedical Research (CSIC-UAB), have confirmed 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. These results are being published in the journal PLoS One.
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", says Héctor Palmer, the coordinator of this study and head of the VHIO's Stem Cells and Cancer laboratory. He continues, "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".
The study was conducted on mice and human colon cancer cells. The mice were used as a model to replicate the initial phases of colon cancer. "These findings show that mice of this kind, which also lack the VDR and hence do not respond to vitamin D, present larger and more aggressive tumours than mice with the VDR", explains Dr. Palmer, and concludes: "The number of tumours is not influenced by the absence of VDR, which would indicate that this factor does not protect against the appearance of the tumour but does intervene in its growth phase, reducing its aggressiveness".
The researchers then 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. These findings were repeated in the three types of colon cancer cells studied, and confirmed the results observed in the mice.