Maitake-polysaccharide enhances apoptosisInduction Effect to Apoptosis by Maitake Polysaccharide: Synergistic Effect of Its Combination With Vitamin C in Neuroglioma Cell.
Combination treatment complicates effects.
We set out to understand how maitake mushroom polysaccharide (MP), when combined with vitamin C (VC), affects brain tumor cells, specifically in human neuroglioma M059 K cells. Through our study, we found that using a combination of MP and VC led to a significant reduction in cell viability—about 53.10%. This indicates that these compounds together may weaken the tumor cells' ability to survive.
Our findings also showed that this combination treatment caused cell cycle arrest at the G2/M phase, meaning that it effectively stopped the cells from proceeding through their natural life cycle. Notably, we observed that 38.54% of the treated cells went through apoptosis, a form of programmed cell death critical for eliminating cancerous cells.
We noted changes in proteins associated with apoptosis, showing upregulation of Bax and caspase-3, while Bcl-2 levels decreased. Additionally, there was an increase in the activities of caspase-3, caspase-8, and caspase-9. These observations suggest that the anticancer effects we witnessed likely stem from the induction of apoptosis triggered by the combined treatment of MP and VC.
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Inositol treatment for brain tumorsInositol treatment inhibits medulloblastoma through suppression of epigenetic-driven metabolic adaptation.
Evaluates inositol's therapeutic potential
We explored the effects of inositol treatment on medulloblastoma, which is a leading cause of brain tumors in children. Specifically, we found that some medulloblastoma cells showed a unique sensitivity to changes in inositol metabolism due to the presence of the BMI1 gene.
Our research focused on a particular sub-group of this tumor that is characterized by a specific gene signature known as BMI1;CHD7. We discovered that treatment with a compound derived from inositol, called IP6, could effectively counteract the aggressive behaviors of these tumors, particularly through blocking the activation of a key metabolic pathway called mTOR.
Additionally, our findings revealed that IP6 does not just work in isolation. When combined with cisplatin, a common chemotherapy drug, IP6 enhanced the drug's ability to kill tumor cells in laboratory settings. This combination also proved beneficial in a pre-clinical model, where it extended survival in mice with tumors that mirrored human medulloblastoma.
Overall, our study suggests that inositol and its derivatives could offer a novel avenue for treatment, particularly for tumors that carry the BMI1;CHD7 signature. However, we emphasize the need for further research to fully understand the potential benefits and mechanisms at play.
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