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.
Dig Liver Dis
; 54(1): 125-135, 2022 Jan.
Article
in En
| MEDLINE
| ID: mdl-34053876
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 ANDRESULTS:
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.Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Transcription Factors
/
Carcinoma, Hepatocellular
/
Homeodomain Proteins
/
MicroRNAs
/
Nuclear Factor 90 Proteins
/
Liver Neoplasms
Limits:
Humans
Language:
En
Journal:
Dig Liver Dis
Journal subject:
GASTROENTEROLOGIA
Year:
2022
Document type:
Article
Affiliation country:
China