Eicosapentaenoic acid impacts tumorsOmega-3 fatty acids decrease CRYAB, production of oncogenic prostaglandin E and suppress tumor growth in medulloblastoma.
We investigated the effects of eicosapentaenoic acid (EPA) alongside docosahexaenoic acid (DHA) on medulloblastoma, a common and aggressive brain tumor in children.
In our study, we treated medulloblastoma cell lines with these omega-3 fatty acids and observed notable changes. Both EPA and DHA significantly reduced the production of prostaglandin E2, a compound associated with tumor growth and inflammation. Furthermore, we saw that these treatments impaired the viability of medulloblastoma cells, meaning fewer cancer cells were able to survive and grow. Additionally, the treatment led to increased cell death and reduced the ability of these cells to form colonies.
When we moved to the in vivo part of our study, where we implanted human medulloblastoma cells into mice, the results were promising. Mice treated with DHA, with or without EPA, experienced reduced tumor growth. Notably, levels of prostaglandin E and another compound, prostacyclin, dropped significantly in the tumors of treated animals compared to those that did not receive treatment. This suggests that the omega-3 fatty acids helped create a less favorable environment for tumor growth.
Our analysis uncovered that the treatment led to a downregulation of several key genes, with CRYAB being the most significantly affected. We confirmed this finding via various techniques, including immunohistochemistry. This research hints at the potential of combining DHA and EPA in existing treatment plans to target inflammation specific to the tumor environment.
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DHA in glioblastoma treatmentPreparation and Evaluation of Mebendazole Microemulsion for Intranasal Delivery: an Alternative Approach for Glioblastoma Treatment.
We investigated the potential of docosahexaenoic acid (DHA) as part of a novel treatment for glioblastoma, a challenging brain tumor. Our study involved formulating mebendazole (MBZ) microemulsions that included DHA along with other compounds, assessing their effectiveness in an orthotopic C6 rat model.
The formulations were carefully characterized before testing. We found that one formulation—composed of oleic acid and labrafil, with a 0.1% mucoadhesive agent—showed promising results. Importantly, there were no observable toxic effects on the nasal epithelium, suggesting the safety of this delivery method.
Furthermore, we observed improved survival rates in the treated rats compared to the control group. Our findings implied that this combined approach with DHA and MBZ microemulsions might offer a new avenue for glioblastoma treatment, although we noted that the contribution of DHA alone couldn't be fully isolated.
Overall, our research encourages the exploration of innovative strategies to enhance the treatment of malignant brain tumors through targeted intranasal delivery.
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EPA enhances cisplatin treatmentEicosapentaenoic acid enhanced apoptotic and oxidant effects of cisplatin via activation of TRPM2 channel in brain tumor cells.
We explored the potential of eicosapentaenoic acid (EPA) in combination with cisplatin (CiSP) as a treatment for brain tumors, specifically glioblastoma cells. Our study involved comparing the effects of different treatments on brain tumor cells, including a control group, EPA treatment, CiSP treatment, and a combination of both.
Our findings indicated that when CiSP was applied, there was a significant increase in calcium responses in the tumor cells, which was crucial for triggering cell death. EPA, known for its oxidant properties due to its high polyunsaturated fatty acid content, further enhanced these responses, leading to increased mitochondrial stress and higher levels of reactive oxygen species.
Not only did EPA boost the effects of CiSP, but it also contributed to increased lipid peroxidation and apoptosis in the tumor cells. These results point out that when we use EPA alongside CiSP, the combined treatment appears to increase the therapeutic effects, making the cancer cells more susceptible to the treatment.
However, we must acknowledge that while the combination treatment showed promise, further research would be necessary to isolate the effects of EPA alone and to confirm its effectiveness in clinical settings. Nonetheless, our study suggests that activating the TRPM2 channel with EPA could be a valuable strategy in treating glioblastoma with Cisplatin.
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Eicosapentaenoic acid shows promiseAssessing fatty acid-induced lipotoxicity and its therapeutic potential in glioblastoma using stimulated Raman microscopy.
Our exploration focused on how eicosapentaenoic acid (EPA) impacts glioblastoma, the most aggressive type of brain tumor. To delve into this, we treated U87 glioma cells with three types of fatty acids: palmitic acid, oleic acid, and EPA. We used a specialized microscope to track how these fatty acids were absorbed by the cells and how they contributed to the formation of lipid droplets.
Interestingly, we found that supplying 200 µM of these fatty acids led to significant accumulation of lipid droplets in the glioma cells. By inhibiting the synthesis of triglycerides, we noticed a depletion of these droplets, which resulted in heightened lipotoxicity. This was marked by a notable reduction in cell proliferation rates.
Most strikingly, when we combined EPA treatment with the depletion of lipid droplets, we observed that it significantly lowered the survival rate of the glioma cells by over 50%. This stark result underscores the potential therapeutic capabilities of this approach. As we look to the future, we are committed to uncovering the metabolic mechanisms behind EPA-induced lipotoxicity, with the aim of enhancing its effects against cancer.
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Eicosapentaenoic acid promotes tumor regressionAntitumour and pro-apoptotic actions of highly unsaturated fatty acids in glioma.
We sought to understand how eicosapentaenoic acid (EPA), a type of highly unsaturated fatty acid, influences brain tumors, specifically gliomas. Using various glioma models, including human samples and a rat model, we looked at how EPA could trigger tumor regression and promote cell death, known as apoptosis.
Our findings revealed that when glioma cells were exposed to EPA, significant reductions in tumor size and increased apoptosis were observed. Furthermore, we noted that EPA worked well in conjunction with gamma radiation, enhancing the effects of this common treatment.
Interestingly, our observations indicated that EPA preserved the surrounding healthy brain tissue and blood vessels, which is a significant consideration in treating brain tumors. We also found minimal inflammation in tumors treated with EPA, suggesting a more favorable safety profile compared to conventional treatments. Overall, the results indicate that EPA could be a promising addition to glioma therapies.
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