LAUSR

The aim of our study is to explore the regulation of C1QTNF1-AS1 on its target miR-221-3p/SOCS3 in human hepatocellular carcinoma (HCC). To explore the underlying molecular regulation of non-coding RNA for HCC, differentially expressed patterns of lncRNAs and genes were examined by RNA-seq. GO and KEGG pathway analysis were done based on the function of mRNAs that mediated by differentially expressed lncRNAs. RT-qPCR and western blot were conducted to detect the mRNA and protein level expression of C1QTNF1-AS1, miR-221-3p, SOCS3 and key proteins in JAK/STAT signaling pathway in HCC tissues and cells. The target miRNA of differentially expressed C1QTNF1-AS1 and SOCS3 was miR-221-3p predicted by bioinformatics analysis. C1QTNF1-AS1 and SOCS3 was downregulated and miR-221-3p was upregulated in HCC tissues and cells. In HepG2 and Huh-7 cells, the overexpression of C1QTNF1-AS1 or SOCS3, and silencing of miR-221-3p inhibited proliferation, migration, invasion and JAK/STAT signaling pathway, while promoted cell apoptosis. The results of dual-luciferase assay indicated that C1QTNF1-AS1 regulated miR-221-3p and miR-221-3p targeted SOCS3 by directly binding. And the growth of HCC in vivo was impeded when C1QTNF1-AS1 was upregulated. Overexpression of C1QTNF1-AS1 could downregulate miR-221-3p thereby inhibited the proliferation, migration and invasion of HCC cells.