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.
Acknowledgment
This study was supported by Sichuan Health and Wellness Committee: Universal application project, (Grant No.: 17PJ593).
Disclosure statement
The authors declare no conflict of interest.