Fructose 1,6-bisphosphatase 1 is a potential biomarker affecting the malignant phenotype and aerobic glycolysis in glioblastoma

• Published in: PeerJ (San Francisco, CA) Vol. 13; p. e18926
• Main Authors: Lu, Weihong, Huang, Guozheng, Yu, Yihan, Zhai, Xia, Zhou, Xiangfeng
• Format: Journal Article
• Language: English
• Published: United States PeerJ. Ltd 31.01.2025; PeerJ Inc
• Subjects: Aerobic glycolysis; Biomarkers, Tumor - genetics; Biomarkers, Tumor - metabolism; Brain Neoplasms - genetics; Brain Neoplasms - metabolism; Brain Neoplasms - pathology; Cell Biology; Cell Line, Tumor; Cell Movement; Cell Proliferation - genetics; Evidence Based Medicine; Fructose; Fructose 1,6-bisphosphatase 1; Fructose-Bisphosphatase - genetics; Fructose-Bisphosphatase - metabolism; Genetic aspects; Glioblastoma; Glioblastoma - genetics; Glioblastoma - metabolism; Glioblastoma - pathology; Glioblastoma multiforme; Glucose metabolism; Glycolysis; Humans; Malignant phenotype; Molecular Biology; Neurology; Oncology; Phenotype; PI3K/AKT pathway; Prognosis; United Kingdom; California; United States; China; Aerobic glycolysis; Fructose 1,6-bisphosphatase 1; Malignant phenotype; Glioblastoma; PI3K/AKT pathway
• ISSN: 2167-8359; 2167-8359
• DOI: 10.7717/peerj.18926

Fructose 1,6-bisphosphatase 1 ( ) has been considered as a potential prognostic biomarker in glioblastoma (GBM), and this study explored the underlying mechanism. The expression and effect of expression on the prognosis of GBM patients were examined applying bioinformatics analyses. After measuring the expression of in normal glial cell line HEB and GBM cells, cell counting kit-8 (CCK-8), 5-ethynyl-2-deoxyuridine (EdU), colony formation, transwell, and wound healing assay were carried out to examine the effects of silencing on the proliferation and invasion of GBM cells. Aerobic glycolysis was measured by calculating the extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) of -silenced GBM cells. Furthermore, the protein levels of the mediators related to PI3K/AKT pathway and protein family were detected immunoblotting. Additionally, the effects of silencing on the macrophage M2 polarization were assessed based on the fluorescence intensity of and the phosphorylation of quantified by immunofluorescence and immunoblotting, respectively. High-expressed was indicative of a worse prognosis of GBM. knockdown in GBM cells suppressed the proliferation, invasion, migration, and aerobic glycolysis of GBM cells, lowered the phosphorylation levels of and and the protein expression of but promoted protein expression. Moreover, knockdown reduced CD206 fluorescence intensity and the phosphorylation of STAT6. To conclude, could be considered as a biomarker that affected the malignant phenotypes and aerobic glycolysis in GBM, contributing to the diagnosis and treatment of GBM.