Guangxin Yan1, Zhihui Chang1, Chuanzhuo Wang1, Zheng Gong1, He Xin1, Zhaoyu Liu2. 1. Department of Radiology, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Heping District, Shenyang 110000, Liaoning, China. 2. Department of Radiology, Shengjing Hospital of China Medical University, No. 36, Sanhao Street, Heping District, Shenyang 110000, Liaoning, China. Electronic address: liuzy1226@126.com.
Abstract
BACKGROUND: Long non-coding RNAs (lncRNAs) are essential indicators for hepatocellular carcinoma. LncRNAs can exert the same functions as their antisense mRNAs. ILF3 is an oncogene in hepatocellular carcinoma. ILF3 divergent transcript (ILF3-AS1) is the antisense RNA of ILF3, and has been reported as an oncogene in various cancers. AIMS: To explore the role of lncRNA ILF3-AS1 in malignant phenotypes of hepatocellular carcinoma cells. METHODS AND RESULTS: RT-qPCR analysis revealed that ILF3-AS1 was significantly upregulated in hepatocellular carcinoma cells. The hepatocellular carcinoma cell viability was suppressed by silenced ILF3-AS1. Transwell and wound healing assays showed that ILF3-AS1 downregulation inhibited cell invasion and migration. The levels of proteins associated with epithelial-mesenchymal transition (EMT) process and the Notch pathway were detected by western blot analysis. Luciferase reporter, RNA pull down and RIP assays were used to investigate the relationship between ILF3-AS1 and downstream target genes. ILF3-AS1 competed with meis homeobox 2 (MEIS2) for miR-628-5p in hepatocellular carcinoma cells. ILF3-AS1 elevated the levels of key proteins on the Notch pathway. Rescue assays demonstrated that MEIS2 reversed the antitumor effects of silenced ILF3-AS1 on hepatocellular carcinoma. In vivo assays demonstrated that ILF3-AS1 silencing inhibited the hepatocellular carcinoma tumor growth. CONCLUSIONS: ILF3-AS1 promoted hepatocellular carcinoma progression via the Notch pathway and miR-628-5p/MEIS2 axis.
BACKGROUND: Long non-coding RNAs (lncRNAs) are essential indicators for hepatocellular carcinoma. LncRNAs can exert the same functions as their antisense mRNAs. ILF3 is an oncogene in hepatocellular carcinoma. ILF3 divergent transcript (ILF3-AS1) is the antisense RNA of ILF3, and has been reported as an oncogene in various cancers. AIMS: To explore the role of lncRNA ILF3-AS1 in malignant phenotypes of hepatocellular carcinoma cells. METHODS AND RESULTS: RT-qPCR analysis revealed that ILF3-AS1 was significantly upregulated in hepatocellular carcinoma cells. The hepatocellular carcinoma cell viability was suppressed by silenced ILF3-AS1. Transwell and wound healing assays showed that ILF3-AS1 downregulation inhibited cell invasion and migration. The levels of proteins associated with epithelial-mesenchymal transition (EMT) process and the Notch pathway were detected by western blot analysis. Luciferase reporter, RNA pull down and RIP assays were used to investigate the relationship between ILF3-AS1 and downstream target genes. ILF3-AS1 competed with meis homeobox 2 (MEIS2) for miR-628-5p in hepatocellular carcinoma cells. ILF3-AS1 elevated the levels of key proteins on the Notch pathway. Rescue assays demonstrated that MEIS2 reversed the antitumor effects of silenced ILF3-AS1 on hepatocellular carcinoma. In vivo assays demonstrated that ILF3-AS1 silencing inhibited the hepatocellular carcinoma tumor growth. CONCLUSIONS: ILF3-AS1 promoted hepatocellular carcinoma progression via the Notch pathway and miR-628-5p/MEIS2 axis.
Authors: Daniel L Pouliquen; Alice Boissard; Cécile Henry; Olivier Coqueret; Catherine Guette Journal: Front Pharmacol Date: 2022-07-08 Impact factor: 5.988