Glucose regulates the HMGB1 signaling pathway through SIRT1 in glioma.

Glucose is a fundamental substance for numerous cancers, including glioma. However, its influence on tumor cells regulatory mechanisms remains uncertain. SIRT1 is a regulator of deacetylation and a key player in the progression of malignant tumors. The objective of this study was to examine the role of glucose and SIRT1 in glioma. This study investigated the association of SIRT1 expression with clinicopathological features and prognosis in glioma patients using the TCGA database. The Western blotting technique was used to identify the expression of SIRT1 protein in glioma cells. The study also examined the impact of differing glucose concentrations on the biological functions of glioma cells. The study investigated the expression of SIRT1 and HMGB1 signaling pathways in glioma. Additionally, resilience experiments were conducted utilizing SRT1720. SIRT1 is a gene that suppresses tumors and is low expressed in gliomas. Low expression of this gene is strongly linked to a poor prognosis in patients with glioma. High concentrations of glucose can promote the proliferation, migration, and invasion of glioma cells, while also inhibiting apoptosis. The findings of this mechanistic study provide evidence that glucose can down-regulate SIRT1 expression, leading to increased levels of acetylated HMGB1. This in turn promotes the ex-nuclear activation of HMGB1 and associated signaling pathways, ultimately driving glioma malignancy. Glucose has the ability to regulate the HMGB1 associated signaling pathway through SIRT1, thus promoting glioma progression. This holds significant research value. • High glucose promotes malignant progression of gliomas and decreases SIRT1 expression. • Activation of SIRT1 inhibits the HMGB1 signaling pathway。 • Glucose promotes glioma progression through SIRT1 regulation of HMGB1 related signaling pathway. [ABSTRACT FROM AUTHOR]