Vitamin B6 as glioblastoma targetVitamin B6 Pathway Maintains Glioblastoma Cell Survival in 3D Spheroid Cultures.
We explored the impact of the vitamin B6 pathway on glioblastoma, a challenging and aggressive brain cancer. Specifically, we assessed how different cell cultures—2D monolayers and 3D spheroids—responded to treatments that alter vitamin B6 levels. Through comprehensive metabolomics analysis, we found notable differences in the levels of vitamin B6-related metabolites between these two culture methods.
Our key finding was that when we used hydralazine, a small molecule known to lower vitamin B6 levels, it induced cell death specifically in the 3D spheroid cultures of glioblastoma. This suggests a potential new therapeutic strategy targeting the vitamin B6 pathway could benefit glioblastoma treatment.
Thus, this study highlights a novel approach to tackle this aggressive cancer by focusing on the metabolic alterations within the tumor microenvironment, particularly through vitamin B6 modulation.
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Pyridoxine promotes glioblastoma apoptosisEffect of pyridoxine or cobalamin supplementation on apoptosis and cell cycle progression in a human glioblastoma cell line.
We explored the impact of vitamin B6, also known as pyridoxine, on the viability and progression of human glioblastoma cells, specifically the U-87 MG cell line. The study involved treating these cells with increasing concentrations of vitamin B6 and monitoring changes over 24 to 72 hours.
Our findings demonstrated that higher doses of pyridoxine resulted in a significant decrease in cell viability, suggesting that it may effectively hinder the growth of glioblastoma. We observed that this reduction in cell viability was likely linked to a slower cell cycle progression and an increase in active caspase 3, a marker of apoptosis or programmed cell death.
Interestingly, while vitamin B6 appeared to enhance the apoptosis process, the levels of Bcl-2, a protein that usually helps cells survive, did not change significantly. Furthermore, when we introduced cobalamin (vitamin B12) alongside pyridoxine, we found that it seemed to counteract some of pyridoxine's harmful effects in terms of cell viability.
Overall, the results imply that vitamin B6 supplementation could potentially be used to promote apoptosis in glioblastoma cells, possibly making it a valuable addition to current cancer therapies.
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