Vitamin D and cisplatin synergyVitamin D promotes anticancer effects of low-concentration cisplatin-treated non-small cell lung cancer cells via inhibiting the JAK2/STAT3 and TGF-β/SMAD4 pathways.
We explored whether adding vitamin D to cisplatin treatment could be a more effective strategy against non-small cell lung cancer (NSCLC). This research focused on how these treatments affect certain critical cellular pathways involved in cancer progression.
The study tested the impact of vitamin D on various cancer cell lines, highlighting that H1299 and A549 cells were particularly responsive. Using techniques like the sulforhodamine-B assay, we discovered that vitamin D treatment significantly altered the expression of genes linked to cancer growth and spread, such as JAK2, STAT3, TGF-β, and SMAD4.
Moreover, when we combined vitamin D with cisplatin, there was a notable decrease in the activity of proteins associated with cancer cell migration and invasion. This combination therapy seems promising as it potentially targets the genes and proteins that enable lung cancer cells to thrive and spread. Overall, the results suggest that vitamin D could enhance the anticancer effects of cisplatin, opening doors for improved treatment strategies for lung cancer patients.
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Vitamin D's role in lung cancerVitamin D-mediated tsRNA-07804 triggers mitochondrial dysfunction and suppresses non-small cell lung cancer progression by targeting CRKL.
We explored the impact of vitamin D treatment on non-small cell lung cancer (NSCLC) and how it may influence mitochondrial functions in cancer cells. By utilizing small RNA sequencing, we identified various tRNA-derived small RNAs (tsRNAs) that were differentially expressed in lung cancer cells treated with vitamin D.
Throughout our experiments, we observed that vitamin D treatment not only led to mitochondrial dysfunction but also suppressed the growth and spread of NSCLC cells. Specifically, we found that a significant increase in a particular tsRNA, known as tsRNA-07804, was linked to the decreased malignancy of these cancer cells.
Further investigations revealed that tsRNA-07804 works by targeting a protein called CRKL, which plays a role in promoting cancer cell survival. This interaction highlights how vitamin D can trigger apoptotic cell death in lung cancer. Our in vivo experiments mirrored these findings, showing reduced tumor growth in response to vitamin D treatment alongside increased tsRNA-07804 levels.
Overall, our research suggests that vitamin D can function as a therapeutic agent by enhancing the expression of tsRNA-07804, ultimately leading to suppressed NSCLC progression. This opens up new avenues for potential treatments in lung cancer patients.
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Vitamin D's potential in lung cancerVitamin D Intake, Serum 25-Hydroxyvitamin-D (25(OH)D) Levels, and Cancer Risk: A Comprehensive Meta-Meta-Analysis Including Meta-Analyses of Randomized Controlled Trials and Observational Epidemiological Studies.
We analyzed various studies examining how vitamin D affects lung cancer, specifically looking at both vitamin D intake and serum levels of 25-hydroxyvitamin D. The findings from 35 eligible meta-analyses revealed a strong link between higher vitamin D intake and reduced lung cancer risk, particularly showing a significant decrease in incidence rates.
Our results indicated that for individuals with higher vitamin D consumption, there was a notable reduction in lung cancer cases. The odds ratio for lung cancer incidence was 0.88, suggesting a potential protective effect. However, when focusing only on randomized controlled trials, the association between vitamin D intake and cancer risk wasn’t significant, indicating that more robust studies could be needed to truly understand this relationship.
Overall, while we see promising evidence that suggests vitamin D may play a beneficial role in lowering lung cancer risk, particularly from observational studies, the randomized controlled trials did not provide substantial backing for this benefit. It’s crucial that we consider factors like cancer type and study design when interpreting these findings.
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Vitamin D3 enhances lung cancer immunity1α,25(OH)D reverses exhaustion and enhances antitumor immunity of human cytotoxic T cells.
We explored the potential role of vitamin D3 in lung cancer patients and its effects on the immune system, specifically focusing on T cells. The research involved 172 patients undergoing treatment for non-small cell lung cancer (NSCLC). These patients received standard chemotherapy and were then given varying doses of vitamin D3 for three weeks.
Our analysis revealed a significant connection between vitamin D levels and immune checkpoint receptors on T cells. Lower levels of vitamin D were associated with higher expressions of exhaustion markers like PD-1 and Tim-3, while higher vitamin D levels correlated with increased CD28 expression, an important marker for T cell activity.
When we looked into the mechanisms of how vitamin D3 works, we found that the active form of vitamin D promotes changes in T cells that help reduce their exhaustion. It does this by influencing specific genes and enhancing T cell function, leading to increased production of Th1 cytokines, which are crucial for effective immune responses against tumors.
Ultimately, we observed that vitamin D3 not only plays a role in improving the function of T cells but also seems to enhance their ability to combat tumor cells in lung cancer patients. This suggests that incorporating vitamin D3 into treatment regimens could potentially improve outcomes for those battling this disease.
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Vitamin D3 inhibits lung cancer growthInhibition of lung cancer by vitamin D depends on downregulation of histidine-rich calcium-binding protein.
We conducted a study to understand how vitamin D3 influences lung cancer, particularly focusing on a protein known as histidine-rich calcium-binding protein (HRC). Our research explored whether vitamin D3 could help lower HRC levels, given its crucial role in calcium balance, which is significant in cancer development.
We measured the expression of HRC and the vitamin D receptor (VDR) in lung cancer tissues compared to normal and adjacent non-cancerous tissues. Using various lab techniques, we assessed how vitamin D3 affects lung cancer cells, including their growth, spread, and ability to undergo programmed cell death, known as apoptosis.
Our findings revealed that vitamin D3 does inhibit the expression of HRC, which in turn decreased the migration and proliferation of lung cancer cells. Additionally, we noted an increase in the number of cells undergoing apoptosis in response to vitamin D3 treatment. In our animal model, mice treated with a vitamin D3 formulation exhibited smaller tumors and fewer cancerous cells than those treated with a combination of vitamin D3 and HRC.
Overall, our study indicates that vitamin D3 plays a protective role against lung cancer by downregulating HRC, thus slowing tumor growth and promoting cancer cell death.
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