Vitamin D cannot function properly without a single gene

Vitamin D is not just a nutrient, but the basis for the production of the important hormone calcitriol. This hormone regulates not only the absorption of calcium and phosphorus in the intestine (which is necessary for bone health), but is also responsible for the immune system, cell growth, muscle and neuron activity.

That is why vitamin D deficiency is associated with an increased risk of cancer, kidney disease, autoimmune and metabolic disorders. But exactly how it gets into the cells and is activated was not completely clear.

Professor Georges Nemer’s group used the CRISPR/Cas9 method to “disable” active SDR42E1 in intestinal cancer cells. As soon as the gene stopped working, the viability of tumor cells decreased by 53%, and the activity of more than 4,000 other genes changed.

Many of these genes are involved in the regulation of cell growth, signaling pathways, and metabolism— especially cholesterol-like substances, which include calcitriol. This indicates the central role of SDR42E1 in the regulation of vital processes.

The use of SDR42E1 is not limited to the fight against cancer. Scientists believe that this gene may be useful in another direction — targeted activation of calcitriol in tissues where it is needed. For example, with chronic inflammation, autoimmune diseases, or metabolic disorders.

“If we learn how to control SDR42E1, it will be possible to fine—tune the work of vitamin D in the body,” emphasizes Professor Nagham Hendy, co-author of the work.

However, the researchers emphasize that further verification and caution are required. Any interference with vitamin D metabolism can affect the overall balance, and the consequences of long—term activation or blocking of SDR42E1 have not yet been fully studied.