Affiliated Hospital of North Sichuan Medical College, Nanchong, China.
The Second Affiliated Hospital of North Sichuan Medical College, Nanchong, China.
Fetal Pediatr Pathol. 2022 Jun;41(3):355-370. doi: 10.1080/15513815.2020.1814915. Epub 2020 Sep 9.
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. 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. 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. FoxM1 knockdown inhibited NB cell proliferation and induced apoptosis through inhibiting activation of PI3K and AKT.
本研究旨在探讨 FoxM1 对神经母细胞瘤（NB）细胞体外生物学行为的影响，以及 FoxM1 与 NB 细胞系中 PI3K/AKT 通路的相关性。通过脂质体转染将重组质粒 pcDNA3.1（+）-FoxM1 和 FoxM1 特异性小干扰 RNA（siRNA）转染至 IMR-32 细胞。通过 qRT-PCR 和 Western blot 检测 FoxM1、AKT 和 PI3K 的表达。通过流式细胞术分析 FoxM1 和 PI3K/AKT 通路对细胞周期和细胞凋亡的影响。通过 CCK8 和集落形成实验评估细胞活力和增殖能力。FoxM1 敲低显著促进 NB 细胞凋亡和 G1 期细胞周期阻滞，增加凋亡相关蛋白的表达，并抑制 PI3K 和 AKT 的磷酸化激活。FoxM1 的过表达则产生相反的效果。FoxM1 敲低通过抑制 PI3K 和 AKT 的激活抑制 NB 细胞增殖并诱导凋亡。
