Apolipoprotein L1 is transcriptionally regulated by SP1, IRF1 and IRF2 in hepatoma cells,FEBS Letters

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Apolipoprotein L1 is transcriptionally regulated by SP1, IRF1 and IRF2 in hepatoma cells
FEBS Letters ( IF 3.0 ) Pub Date : 2020-07-28 , DOI: 10.1002/1873-3468.13887
De-Ping Wang _{1,

2,

3} , Zhao-Xi Yu ₁ , Zong-Cun He ₂ , Jin-Fu Liao ₂ , Xue-Bin Shen _{2,

4} , Peng-Li Zhu ₁ , Wan-Nan Chen ₂ , Xu Lin ₂ , Shang-Hua Xu ₄

Affiliation

Apolipoprotein L1 (APOL1) participates in lipid metabolism. Here, we investigate the mechanisms regulating APOL1 gene expression in hepatoma cells. We demonstrate that the −80‐nt to +31‐nt region of the APOL1 promoter, which contains one SP transcription factor binding GT box and an interferon regulatory factor (IRF) binding ISRE element, maintains the maximum activity. Mutation of the GT box and ISRE element dramatically reduces APOL1 promoter activity. EMSA and chromatin immunoprecipitation assay reveal that the transcription factors Sp1, IRF1 and IRF2 could interact with their cognate binding sites on the APOL1 promoter. Overexpression of Sp1, IRF1 and IRF2 increases promoter activity, leading to increased APOL1 mRNA and protein levels, while knockdown of Sp1, IRF1 and IRF2 has the opposite effects. These results demonstrate that the APOL1 gene could be regulated by Sp1, IRF1 and IRF2 in hepatoma cells.

中文翻译：

肝癌细胞中载脂蛋白 L1 受 SP1、IRF1 和 IRF2 转录调控

载脂蛋白 L1 (APOL1) 参与脂质代谢。在这里，我们研究了肝癌细胞中 APOL1 基因表达的调节机制。我们证明，APOL1启动子的-80-nt至+31-nt区域包含一个SP转录因子结合GT盒和一个干扰素调节因子（IRF）结合ISRE元件，保持了最大活性。 GT 盒和 ISRE 元件的突变会显着降低 APOL1 启动子活性。 EMSA 和染色质免疫沉淀分析表明转录因子 Sp1、IRF1 和 IRF2 可以与其 APOL1 启动子上的同源结合位点相互作用。 Sp1、IRF1和IRF2的过表达会增加启动子活性，导致APOL1 mRNA和蛋白水平增加，而Sp1、IRF1和IRF2的敲低则会产生相反的效果。这些结果表明肝癌细胞中APOL1基因可以受到Sp1、IRF1和IRF2的调控。

更新日期：2020-07-28

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