Increasing evidence indicates that miR-429 is involved in tumor suppression in various human cancers. However, its role in liver regeneration remains unexplored. Liver regeneration is a highly orchestrated process that can be regulated by microRNAs (miRNAs), although the mechanisms are largely unclear. In this study, we aimed to identify the role of miR-429 in hepatocyte proliferation during liver regeneration. First, we performed microarray analysis and qRT-PCR. Results indicated that miR-429 level in rat liver markedly decreased 30 h after partial hepatectomy, and miR-429 overexpression disrupted BRL-3A proliferation and the transition of G1 to S phase in rat hepatocyte and promoted hepatocyte apoptosis. By contrast, miR-429 down-regulation had inverse effects. MiR-429 negatively regulated JUN expression in vitro and in vivo. After using JUN siRNA, we found that JUN inhibition mediates the effect of miR-429 in hepatocyte proliferation and growth and miR-429 negatively regulates JUN/MYC/BCL2/CCND1 signaling pathways. Our results also indicated that miR-429 inhibits hepatocyte proliferation and liver regeneration by targeting JUN/MYC/BCL2/CCND1.

越来越多的证据表明，miR-429参与了各种人类癌症的肿瘤抑制。然而，其在肝再生中的作用仍未探索。肝脏再生是一个高度协调的过程，可以通过microRNA（miRNA）进行调节，尽管机理尚不清楚。在这项研究中，我们旨在确定miR-429在肝再生过程中在肝细胞增殖中的作用。首先，我们进行了微阵列分析和qRT-PCR。结果表明，部分肝切除术后30 h，大鼠肝脏miR-429水平明显降低，miR-429的过表达破坏大鼠肝细胞中BRL-3A的增殖和G1向S期的转变，并促进肝细胞凋亡。相比之下，miR-429下调具有相反的作用。在体外和体内，MiR-429均负调控JUN表达。使用JUN siRNA后，我们发现JUN抑制作用介导miR-429对肝细胞增殖和生长的作用，而miR-429负调控JUN / MYC / BCL2 / CCND1信号通路。我们的结果还表明，miR-429通过靶向JUN / MYC / BCL2 / CCND1抑制肝细胞增殖和肝脏再生。