[No authors listed]
This study aims to investigate the role of long noncoding RNA SNHG20 in the progression of nonalcoholic fatty liver disease (NALFD) to hepatocellular carcinoma (HCC), and to elucidate whether polarization of Kupffer cells (KCs, liver macrophages) was involved in this process. Mouse NALFD was induced by 16âweeks of high-fat diet (HFD) feeding. Mouse NALFD-HCC was induced by 36âweeks of HFD feeding (from 1âweek to 36âweeks) and 20âweeks of diethyl nitrosamine (DEN) administration (from 17âweeks to 36âweeks). The LV-shRNA- and LV-sh-SNHG20-infected RAW264.7 cells were injected into the NALFD mice followed by DEN treatment to evaluate the role of SNHG20 in regulating the progression of NALFD to HCC in mice. The proportion of M1 and M2 macrophages was determined by flow cytometry. The levels of M1-related inducible nitric oxide synthase (iNOS) and tumor necrosis factor-α and M2-related Arg-1 and interleukin (IL)-10 were also examined. SNHG20 expression was decreased in NALFD but increased in NALFD-HCC, both in human and experimental mouse livers. Furthermore, human and mouse NALFD-HCC KCs displayed decreased M1/M2 ratio compared with NALFD KCs. Moreover, SNHG20 overexpression induced M2 polarization through activating whereas SNHG20 silencing suppressed M1 polarization in RAW264.7 macrophages and delayed the progression of NALFD to HCC in mice. SNHG20 may facilitate the progression of NALFD to HCC via inducing liver KCs M2 polarization via activation.
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