AICAR通过激活Foxc1信号抑制小鼠F9细胞增殖

AICAR Represses the Proliferation of Mouse F9 Cell by Activating Foxc1 Signaling

为了探索5-氨基咪唑-4-氨甲酰核糖核苷(AICAR)抑制小鼠F9细胞(F9 embryonal carcinoma cells)增殖的作用机制,本文构建了Foxc1的慢病毒真核表达载体,通过实时定量PCR、免疫荧光染色、双荧光素酶报告基因检测系统以及细胞增殖检测试验,探索AICAR抑制小鼠F9细胞的增殖作用机制.结果发现,AICAR可以在RNA和蛋白水平促进Foxc1的基因表达,并可以作用于核转录因子κB通路.另外在培养液中添加AICAR或过表达Foxc1都能抑制F9细胞的增殖.信号通路报告载体检测发现Foxc1可以激活核转录因子κB通路以及细胞周期相关的通路.总之,本研究证明,AICAR通过激活Foxc1通路及其下游多条信号通路来抑制F9细胞增殖.

This study aimed to explore the effects of 5-aminoimidazole-4-carboxamide ribonucleoside （AICAR） on F9 embryonal carcinoma cell proliferation and the related mechanism. We constructed an eukaryotic Foxcl expression plasmid and used for transient transfection. The qPCR and immunofluorescence experiments indicated that Foxcl was activated after treatment of AICAR. Dual luciferase reporter （DLR） and cell proliferation assay showed that AICAR treatment or overexpression of Foxcl involved the activation of NF-s：B signal pathway, cell cycle related signal pathway to repress cell proliferation. The results indicated that AICAR treatments resulted in the activation of Foxcl transcription factor, and several signal pathways to affect mouse F9 cell proliferation.