We examined how a selenium-containing drug, known as RuSe, targets cancer cells while sparing normal cells. This innovative approach leverages the unique properties of selenium, specifically its electrophilic center, to create oxidative stress within cancer cells. By shuttling electrons from biological electron donors, the drug activates a sequence of events detrimental to cancer survival.
The results were striking; we found that the rate of electron transfer at the selenium site is significantly higher in cancer cells compared to normal cells—1.81 times greater, to be precise. This selective action leads to a lethal effect, with the drug being 14.98 times more harmful to cancer cells than to their healthy counterparts. We observed that the generation of superoxide anions from this process causes DNA damage and triggers the p53 signaling pathway, which enhances the drug's effectiveness in killing cancer cells.
Our findings offer an exciting new avenue for crafting chemotherapeutic agents that can be both efficient and less toxic. By exploiting the special properties of selenium, we open the door to more intelligent and targeted cancer therapies that could reduce side effects for patients.
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We examined the potential of a specific β-glucan, GFPBW1, derived from maitake mushrooms to enhance the effectiveness of cancer vaccines. The study involved the use of OVA-antigen and a B16-OVA tumor model to see how GFPBW1 might improve immune responses.
Our findings indicated that different doses of GFPBW1 significantly boosted the activation and maturation of immune cells known as antigen presenting cells (APCs). By increasing important markers, we observed greater immune responses, which included higher levels of OVA-specific antibody subtypes like IgG1 and IgG3. This suggests that GFPBW1 could effectively work as an adjuvant, facilitating both Th1 (cell-mediated) and Th2 (humoral) immune responses, which are crucial in fighting cancer.
Additionally, we noted that when GFPBW1 was combined with aluminum, commonly used in vaccines, it led to even higher levels of specific antibodies, creating a balanced immune response. Importantly, the mice that received GFPBW1 with the vaccine did not show any harmful side effects.
In tumor models, GFPBW1 demonstrated remarkable potential in suppressing tumors when used in preventive settings and also enhanced the effects of therapeutic vaccines. The research highlighted a significant increase in targeting immune cells directly to the tumor environment, which illustrates the beneficial role GFPBW1 could play in both vaccine development and cancer therapy.
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We aimed to understand the impact of selenium-enriched Akkermansia muciniphila (Se-AM) on colon cancer, specifically looking at its effectiveness in treating tumors in mice. By enriching the probiotics with inorganic selenium, we prepared Se-AM and evaluated its performance against colon cancer cells using a mouse model.
Our findings revealed that Se-AM was effective in killing colon cancer cells, notably the CT26 cells. The effectiveness seemed to depend on the concentration, indicating that higher doses were better at destroying these cancer cells. In addition to this direct killing effect, we saw that Se-AM played a therapeutic role in mice with established tumors by reducing tumor size and positively altering inflammatory markers in the colon.
Importantly, treatment with Se-AM restored gut microbiota diversity back to levels similar to healthy controls. We observed a notable increase in beneficial bacteria, which suggests that Se-AM not only addresses cancer cells but also promotes a healthier gut environment. Furthermore, we didn't find any adverse effects on vital organs in the mice, highlighting the safety of this treatment.
Overall, our work indicates that Se-enriched Akkermansia muciniphila has promising potential in the fight against colon cancer, providing both direct anti-cancer effects and supporting gut health.
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Selenium nanoparticles show cancer potentialLuminescent Biogenic Selenium Nanoparticles From Indigofera aspalathoides Vahl ex DC: A Novel Hepatoprotective Strategy for Enhancing Live Health.
High relevance in cancer therapy
We focused on the potential of selenium nanoparticles (SeNPs) derived from the medicinal plant Indigofera aspalathoides in treating cancer, particularly its hepatoprotective capabilities. In our exploration, we utilized an ethanolic extract of the plant to green-synthesize SeNPs and then characterized them using several analytical techniques.
The particle sizes were found to be between 50-80 nm, ensuring they are both stable and effective for biological interactions. We evaluated their antioxidant activity and cytotoxic effects, particularly on breast cancer (MCF-7) and liver cancer (HepG2) cell lines. The SeNPs exhibited impressive antioxidant properties, with a DPPH scavenging rate of 70.32% and hydroxyl radical scavenging at 73.68%.
Notably, we discovered that the SeNPs provided significant protection to liver cells at a concentration of 88 μg/mL, maintaining 100% cell viability. However, we also identified that higher selenium concentrations could lead to cytotoxicity. Our findings highlight selenium nanoparticles as promising candidates for addressing oxidative stress and liver-related disorders while offering potential benefits in cancer treatment.
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We synthesized thirty selenium-containing coumarin derivatives and tested their effectiveness against various malignant tumor cell lines. Notably, one compound, referred to as 11i, showed remarkable potency against SK-N-SH neuroblastoma cells, with a low inhibitory concentration of just 2.5 μM.
Our experiments demonstrated that compound 11i significantly inhibited not only cell proliferation but also migration and invasion. Through several analyses, we observed an increase in the Bax/Bcl-2 protein expression ratio, which is a marker for apoptosis, alongside the release of Cytochrome C from the mitochondria. This process triggered apoptosis via the mitochondria-mediated pathway, effectively inducing cell death in neuroblastoma.
Moreover, we noted that the compound localized within the cytoplasm and interacted closely with mitochondria, suggesting it may disrupt normal mitochondrial functions. Computational docking studies supported these findings, showing that compound 11i bound strongly to Bcl-2 and mitochondrial G-quadruplexes.
In in vivo studies, using a mouse model of neuroblastoma, compound 11i exhibited impressive anti-tumor effects, achieving tumor inhibition rates of 79% and 93% at doses of 10 and 20 mg/kg, respectively. These results indicate the potential of selenium-containing coumarin derivatives as promising candidates for developing new treatments against neuroblastoma.
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