A novel therapeutic strategy for antifibrotic based on a new gene NS5ATP9

For several decades, our group was committed to studying of these 127 new genes, providing a new research perspective for liver diseases. Hepatitis C virus core protein-binding protein 6 (HCBP6) upregulates sterol regulatory element-binding protein 1c (SREBP1c) expression by binding to the C/EBPβ-binding site in the SREBP1c promoter [3] and then modulating intracellular triglyceride homeostasis [4]. Hepatitis C virus nonstructural protein 5A trans-activated protein 6 (NS5ATP6) regulates the intracellular triglyceride level via fibroblast growth factor 21 (FGF21), and independently of sirtuin1 (SIRT1) and SREBP1 [5]. HCV promotes the profibrogenic effect of HCV NS5A-transactivated protein 13 (NS5ATP13), by transforming growth factor β1/Sekelsky mothers against decapentaplegic homolog 3 (TGFβ1/Smad3) and nuclear factor κB (NF-κB) signal pathways. Moreover, as a pro-fibrogenic factor, NS5ATP13 expression is down-regulated by CX-4945, a CK2 specific inhibitor [6]. Besides, NS5ATP13 promotes the proliferation and migration of HepG2 cells (human hepatoblastoma HepG2 cell line). Also, oxymatrine (OMT) may inhibit liver cancer progression by downregulating NS5ATP13 expression [7]. Hepatitis C virus nonstructural protein 5A-associated binding protein 37 (NS5ABP37) inhibits cancer cell proliferation and promotes its apoptosis, by altering SREBP-dependent lipogenesis and cholesterogenesis and inducing oxidative stress and endoplasmic reticulum stress [8]. In HCC, hepatitis B virus X Ag-transactivated protein 8 (XTP8) acts as a valuable prognostic predictor by forming a positive feedback loop with FOXM1 oncogene [9]. Hepatitis C virus p7 trans-regulated protein 3 (p7TP3), the direct target gene of miR-182-5p, inhibits HCC by Abstract