Daijiworld Media Network - New Delhi

New Delhi, Jul 19: In a breakthrough that could reshape treatments for cancer and autoimmune diseases, scientists have discovered a gene critical for vitamin D absorption — with the potential to selectively destroy cancer cells. The gene, named SDR42E1, plays a vital role in absorbing and metabolising vitamin D in the human body.

The study, published in the journal Frontiers in Endocrinology, suggests that blocking or inhibiting SDR42E1 could disrupt cancer cell survival while sparing healthy cells. “Our findings show that targeting SDR42E1 may selectively halt cancer growth,” said Dr Georges Nemer, Professor at the College of Health and Life Sciences, Hamad Bin Khalifa University, Qatar.

Previous research had already linked a mutation in the SDR42E1 gene — located on chromosome 16 — to vitamin D deficiency. This mutation results in a truncated, inactive protein that can no longer assist in vitamin D processing.

Using CRISPR/Cas9 gene-editing technology, the researchers transformed the active SDR42E1 gene into its inactive form in HCT116, a human colorectal cancer cell line. Normally, these cancer cells express SDR42E1 abundantly, hinting at the gene’s importance for their survival.

The results were striking: once the faulty gene was introduced, cancer cell viability dropped by 53%, suggesting a targeted, gene-specific approach to cancer treatment may be possible.

“This opens exciting possibilities in precision oncology, although further clinical studies are essential before we can translate it into actual therapies,” said Dr Nagham Nafiz Hendi, Professor at Middle East University in Amman, Jordan.

Because SDR42E1 is tied to vitamin D metabolism, the gene could also become a therapeutic target for other diseases where vitamin D plays a key regulatory role — including autoimmune and metabolic disorders.

However, researchers caution that long-term effects on overall vitamin D balance remain unclear. “We must understand more about how SDR42E1 impacts systemic vitamin D function before moving forward,” Nemer added.

The findings mark a promising step toward personalised medicine and gene-based therapies, but much work remains before the approach reaches clinical application.