Genetic association of vitamin D and cancer risk
The SDR42E1 gene, a key player in vitamin D metabolism, has been linked to cancer cell viability. This gene is instrumental in converting vitamin D into its active hormonal form, calcitriol, which is essential for cellular health and immune regulation.
Recent research has identified a specific mutation that inactivates SDR42E1, leading to vitamin D deficiency and significantly reducing the viability of colorectal cancer cells (HCT116), decreasing their survival by about 53%.
Key findings about SDR42E1 reveal that it acts as a crucial molecular switch for several pathways, disrupting over 4,600 downstream genes involved in cancer-related signaling and cholesterol-like molecule metabolism. Inhibiting SDR42E1 selectively kills cancer cells by depriving them of vitamin D, a strategy that could potentially be harnessed for precision oncology therapies.
The SDR42E1 gene also influences the expression of proteins associated with cell proliferation, nutrient transport, tumor suppression, and drug resistance, pointing to its broader impact on cancer progression and therapy response.
In the VITAL study, people with a normal body mass index could expect a higher risk reduction for developing advanced cancer than those with a higher BMI. Several factors, such as body mass index, age, sex, and cholesterol levels, can impact a person's ability to make and maintain vitamin D. Approximately 35% of adults in the U.S. have a vitamin D deficiency.
It's worth noting that vitamin D is significantly important for bone health, cell growth, muscle function, nerve cell function, and the immune system. The active form of SDR42E1, when transformed into its inactive form in a line of cancer cells called HCT116, caused a 53% decrease in the viability of the cancer cells.
Exposure of 25% of the body to sunlight for 8 to 10 minutes at noon in spring and summer produces the recommended amount of vitamin D. However, it takes more time in the winter to synthesize vitamin D from sunlight: nearly 2 hours of sun exposure at noon to produce vitamin D if just 10% of the body is exposed.
The SDR42E1 gene, when mutated, can cause the protein to be inactive. This mutation has been linked to vitamin D deficiency. Nutrition studies have indicated that increasing vitamin D levels could lower the risk of cancer, kidney disease, autoimmune, and metabolic disorders.
In summary, SDR42E1 is a vital regulator of vitamin D metabolism and a key factor in supporting the survival and growth of cancer cells. Its role makes it a promising target in cancer treatment strategies linked to vitamin D pathways. Further research is needed to explore the potential of SDR42E1 as a therapeutic target in cancer treatment.
Read also:
- Explored the Popular Health Assessment with a Queue of 100,000 Aspiring Participants - Here's My Unadulterated Opinion
- Hearing impairment condition: Recognizing symptoms and management approaches
- Signs of Cataracts Emergence: Impact on Vision and Further Details
- Thrombocytopenia in Large Scale: Root Causes, Identifiable Symptoms, and Available Treatment Options
