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

FEBS Letters

article

De-Ping Wang¹  Zhao-Xi Yu¹  Zong-Cun He²  Jin-Fu Liao²  Xue-Bin Shen²  Peng-Li Zhu¹  Wan-Nan Chen²  Xu Lin²  Shang-Hua Xu⁴ 

[1] Department of Medical Intensive Care Unit, Fujian Provincial Hospital, Provincial Clinical Medical College of Fujian Medical University;Key Laboratory of Gastrointestinal Cancer (Fujian Medical University), Ministry of Education, School of Basic Medical Sciences, Fujian Medical University;Department of Endocrinology and Metabolism, Hongqi Hospital of MuDanJiang Medical College;Department of Cardiology, Affiliated Nanping First Hospital, Fujian Medical University

关键词: apolipoprotein L1;    Promoter;    SP1;    IRF1;    IRF2;   

DOI  :  10.1002/1873-3468.13887

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

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