One tiny gene helps us absorb vitamin D—and may also be the secret to shutting down cancer.
Scientists
have found a surprising connection between vitamin D and a single gene called
SDR42E1.
This gene helps the body absorb
vitamin D—which is important for bones, muscles, and immunity—but researchers
discovered it also plays a powerful role in cancer. When they switched the gene
off in cancer cells, the tumors stopped growing. This breakthrough could lead
to new treatments that either block the gene to fight cancer or boost it to
improve health in other conditions like autoimmune diseases.
Vitamin D’s Critical Role in the
Body
Vitamin
D is widely known as a vital nutrient, but it also plays another critical role.
It serves as the building block for calcitriol, a hormone that helps the body
absorb calcium and phosphate—minerals that are essential for strong bones.
Calcitriol also supports healthy muscle and nerve function, regulates cell
growth, and plays a crucial role in maintaining the proper functioning of the
immune system.
In a
new study published in Frontiers in Endocrinology,
scientists have identified a gene called SDR42E1 as
essential for how the body absorbs vitamin D through the digestive system and
processes it further. This finding could have major implications for targeted
treatments, especially in areas like cancer care.
“Here
we show that blocking or inhibiting SDR42E1 may
selectively stop the growth of cancer cells,” said Dr. Georges Nemer, a
professor and associate dean for research at the University of College of
Health and Life Sciences at Hamad Bin Khalifa University in Qatar, and the
study’s corresponding author.
The Broken Gene That Led to a
Breakthrough
The
research team was motivated by previous studies that linked a specific mutation
in the SDR42E1 gene, located on chromosome 16, with vitamin D
deficiency. This mutation shortened the gene’s protein product, rendering it
inactive.
To
explore its role further, the team used CRISPR/Cas9 gene-editing technology to
deactivate SDR42E1 in a colorectal cancer cell line known as HCT116. These
cells typically exhibit high levels of SDR42E1, suggesting that the gene may be
crucial for their survival. Once the gene was inactivated, the cancer cells
were no longer able to thrive.
Thousands of Genes Respond—And
Tumors Shrink
Once
the faulty SDR42E1 copy had been introduced, the viability of the
cancer cells plummeted by 53%. No fewer than 4,663 ‘downstream’ genes changed
their expression levels, suggesting that SDR42E1 is
a crucial molecular switch in many reactions necessary for the health of cells.
Many of these genes are normally involved in cancer-related cell signaling and
the absorption and metabolism of cholesterol-like molecules – consistent with
the central role of SDR42E1 in
calcitriol synthesis.
These
results suggest that inhibiting the gene can selectively kill cancer cells,
while leaving neighboring cells unharmed.
A Two-Way Street: Fighting Cancer
or Boosting Health
“Our
results open new potential avenues in precision oncology, though clinical
translation still requires considerable validation and long-term development,”
said Dr. Nagham Nafiz Hendi, a professor at Middle East University in Amman,
Jordan, and the study’s first author.
But
starving selected cells of vitamin D is not the only possible application that
immediately sprang to the mind of the researchers. The present results suggest
that SDR42E1 cuts two ways: artificially ‘dialing up’
levels of SDR42E1 in local tissues through gene technology might
likewise be beneficial, leveraging the many known health effects of calcitriol.
Could Boosting the Gene Help in
Other Diseases?
“Because SDR42E1 is involved in vitamin D metabolism, we could
also target it in any of the many diseases where vitamin D plays a regulatory
role,” said Nemer.
“For
example, nutrition studies have indicated that the hormone can lower the risk
of cancer, kidney disease, and autoimmune and metabolic disorders.”
“But
such broader applications must be done with caution, as long-term effects
of SDR42E1 on vitamin D balance remain to be fully
understood,” warned Hendi.
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