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The Mechanism Study of Intermittent Fasting in Glioblastoma Suppression via Gut Microbiota-mediated m6A Modification

ABSTRACT: Glioblastoma Multiforme (GBM) is one of the most malignant tumors, characterized by high treatment costs and poor outcomes, thus urgently necessitating the development of new therapeutic approaches. Recent studies have found that intermittent fasting (IF) not only can suppress GBM among various tumors but also can reconstruct the gut microbiome and alter metabolism. However, the mechanism by which IF inhibits GBM is not yet fully understood. Using animal models, I discovered that IF can effectively suppress GBM and alter the gut microbiome. Furthermore, microbial metabolites such as methionine, m6A, and the m6A-targeted oncogene TGFB2 were also downregulated. Therefore, we hypothesize that IF, by reconstructing the gut microbiome, reduces the levels of microbial metabolite methionine, subsequently decreasing m6A in GBM, leading to the downregulation of the m6A-targeted oncogene TGFB2, thereby inhibiting the development of GBM.

ORGANISM(S): Mus musculus

PROVIDER: GSE274697 | GEO | 2025/07/31

REPOSITORIES: GEO

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Project description:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.

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The Mechanism Study of Intermittent Fasting in Glioblastoma Suppression via Gut Microbiota-mediated m6A Modification

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