1. LncRNA ILF3-AS1 promotes cell migration, invasion and EMT process in hepatocellular carcinoma via the miR-628–5p/MEIS2 axis to activate the Notch pathway
- Author
-
Zheng Gong, He Xin, Guangxin Yan, Zhaoyu Liu, Zhihui Chang, and Chuanzhuo Wang
- Subjects
Carcinoma, Hepatocellular ,Epithelial-Mesenchymal Transition ,Notch signaling pathway ,03 medical and health sciences ,0302 clinical medicine ,Downregulation and upregulation ,Cell Movement ,Cell Line, Tumor ,Humans ,Medicine ,Gene silencing ,Neoplasm Invasiveness ,RNA, Antisense ,Nuclear Factor 90 Proteins ,Homeodomain Proteins ,Receptors, Notch ,Hepatology ,Oncogene ,business.industry ,Liver Neoplasms ,Gastroenterology ,RNA ,Cell migration ,medicine.disease ,Antisense RNA ,MicroRNAs ,Phenotype ,030220 oncology & carcinogenesis ,Hepatocellular carcinoma ,Cancer research ,RNA, Long Noncoding ,030211 gastroenterology & hepatology ,business ,Transcription Factors - 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.
- Published
- 2022