FoxM1 Regulates Proliferation and Apoptosis of Human Neuroblastoma Cell through PI3K/AKT Pathway. (1st June 2022)

• Record Type: Journal Article
• Authors: Liao, Junzuo; Jiang, Lin; Wang, Cheng; Zhao, Dan; He, Wenfei; Zhou, Kejun; Liang, Yun
• Is Part Of: Fetal and pediatric pathology. Volume 41:Number 3(2022)
• Page Start: 355
• Page End: 370
• Publication Date: 2022-06-01
• Subjects: Apoptosis -- FoxM1 -- neuroblastoma -- PI3K/AKT pathway -- proliferation; Pathology, Molecular -- Periodicals; Pediatrics -- Periodicals; Molecular biology -- Periodicals; Pediatric pathology -- Periodicals; Fetal Diseases -- pathology -- Periodicals; Infant, Newborn, Diseases -- pathology -- Periodicals; Pediatrics -- Periodicals; 618.92007
• DOI: 10.1080/15513815.2020.1814915
• Languages: English
• ISSNs: 1551-3815

Abstract

Abstract: Aim: This study investigated the effect of FoxM1 on the biological behavior of neuroblastoma (NB) cells in vitro and the association between FoxM1 and PI3K/AKT pathways in NB cell lines. Materials and methods: Recombinant plasmid pcDNA3.1 (+)-FoxM1 and FoxM1-specific small interfering RNA (siRNA) were transfected into IMR-32 cells by liposome transfection. The expression of FoxM1, AKT and PI3K were determined by qRT-PCR and western blotting. The effect of FoxM1 and PI3K/AKT pathways on the cell cycles and apoptosis were analyzed by flow cytometry. Cell viability and proliferation ability were assessed by CCK8 and colony formation assay. Results: Knockdown of FoxM1 promoted NB cell apoptosis and G1-phase cell cycle arrest significantly, increased the expression of apoptosis-related proteins, and suppressed the phospho-activation of PI3K and AKT. Over-expression of FoxM1 had the opposite effects. Conclusion: FoxM1 knockdown inhibited NB cell proliferation and induced apoptosis through inhibiting activation of PI3K and AKT.