Published online Jul 26, 2022. doi: 10.4252/wjsc.v14.i7.539
Peer-review started: March 6, 2022
First decision: April 19, 2022
Revised: April 24, 2022
Accepted: June 22, 2022
Article in press: June 22, 2022
Published online: July 26, 2022
Processing time: 141 Days and 20.7 Hours
Cancer stem cells (CSCs) have been implicated in tumorigenesis and tumor recurrence and metastasis are key therapeutic targets in cancer treatment. MicroRNAs display therapeutic potential by controlling the properties of CSCs; however, whether an association exists between miR-3682-3p and CSCs is unknown.
However, whether an association exists between miR-3682-3p and CSCs is unknown. Here, we investigated whether miR-3682-3p has a role in hepatocellular carcinoma (HCC).
To investigate the mechanism by which miR-3682-3p promotes stemness maintenance in HCC.
MiR-3682-3p expression in HCC cell lines and 34 pairs of normal and HCC specimens was assayed by qPCR. The functional role of miR-3682-3p was investigated in vitro and in vivo. Dual-luciferase reporter and chromatin immunoprecipitation assays were performed for target assessment, and western blotting was utilized to confirm miR-3682-3p/target relationships.
We found that miR-3682-3p plays a key role in HCC pathogenesis by promoting HCC cell stemness. The upregulation of miR-3682-3p enhanced CSC spheroid-forming ability, side population cell fractions, and the expression of CSC factors in HCC cells in vitro and the tumorigenicity of transplanted HCC cells in vivo. Furthermore, silencing miR-3682-3p prolonged the survival of HCC-bearing mice. Mechanistically, we found that miR-3682-3p targets FOXO3 and enables FOXO3/β-catenin interaction, which promotes c-Myc expression through PI3K/AKT; c-Myc, in turn, activates miR-3682-3p, forming a positive feedback loop. Intriguingly, miR-3682-3p expression was induced by hepatitis B virus X protein (HBx) and was involved in HBx-induced tumor stemness-related pathogenesis.
Our findings reveal a novel mechanism by which miR-3682-3p promotes stemness in HCC stem cells. Silencing miR-3682-3p may represent a novel therapeutic strategy for HCC.
This study has shed some light on the mechanism of action of miR-3682-3p in promoting stemness maintenance in HCC and provides a potential target for the treatment of HCC.