Vitamin D3 is such a familiar nutrient that it is easy to forget how important it is for critical reasons. Unfortunately, many people are deficient in vitamin D.
Additionally, people may have issues with a cellular transcription factor called “vitamin D receptor” (VDR). VDR is one of the many factors in the body that regulates the way cells reproduce. As you may guess, it is activated by vitamin D3. If there are any problems with this system, a person may need higher levels of vitamin D3 in their regimen than what is considered the average daily allowance.
This study found that vitamin D3 suppressed gastric tumor growth in studies of patient cancer cells and in mice bearing tumors as well. One of the ways vitamin D3 worked was by reducing the expression of a glycoprotein called CD44. CD44 can cause the conglomeration of cells that form tumors, so finding a readily available nutrient that can stop them is excellent news. The authors conclude that vitamin D3 may have potential as a low-cost preventive medicine and treatment for gastric cancer.
One thing to bear in mind is that vitamin D3 (cholecalciferol) is available as a supplement and is already in the form that the body needs, unlike vitamin D2, which requires conversion into that form.
Li Q, Li Y, Jiang H, et al. Vitamin D suppressed gastric cancer cell growth through downregulating CD44 expression in vitro and in vivo. Nutrition. 2021; 111413.
Objectives: Vitamin D deficiency was found being associated with increased gastric cancer (GC) risk. We previously found that vitamin D inhibited GC cell growth in vitro. However, the in vivo antitumor effect of vitamin D in GC as well as the underlying mechanisms are not well understood. The aim of this study is thus to investigate the anticancer effect of vitamin D on GC both in vitro and in vivo.
Methods: Human gastric cancer cells MKN45, MKN28 and KATO III cells were used. The expressions of VDR and CD44 were downregulated by using pre-designed siRNA molecules. Cell viability was evaluated by MTT assay. Soft agar assay was used for colony formation of GC cells. Flow cytometry was used to assess CD44 positive cell population. CD44high cancer cells were enriched by using anti-CD44-conjugated magnetic microbeads. Quantitative real-time PCR and western blot were performed to detect gene and protein expressions respectively. Clinical samples were collected for evaluation of the correlation of vitamin D receptor (VDR) and CD44 expression. Orthotopic tumor bearing mice were established to evaluate the antitumor effect of vitamin D.
Results: The results showed that the active form of vitamin D, 1,25(OH)2D3, had a remarkable inhibitory effect in CD44-expressing human GC MKN45 and KATO III cells, but not in CD44-null MKN28 cells. The gene expressions of CD44 and VDR in GC cell lines and GC patient tissues were positively correlated. Furthermore, 1,25(OH)2D3 suppressed MKN45 and KATO III cell growth through VDR-induced suppression of CD44. In addition, we demonstrated that 1,25(OH)2D3 inhibited Wnt/β-catenin signaling pathway which might led to the downregulation of CD44. In orthotopic GC nude mice model, both oral intake of vitamin D and i.p. injection with 1,25(OH)2D3 could significantly inhibit orthotopic GC growth and CD44 expression in vivo.
Conclusion: We provided the first evidence that vitamin D suppressed gastric cancer cell growth both in vitro and in vivo through downregulating CD44. Current study sheds light on repurposing vitamin D as a potential therapeutic agent for GC prevention and treatment.
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