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Article Abstract
Background: This research study explores the effect of miR-361 on the activation of immortalized human and mice hepatic stallate cells (HSCs).
Methods: 10 liver specimens from healthy volunteers and 20 HBV-relevant HCC tissues from patients. The expressions of miR-361 in HCC patients, HBx transgenic mice, HCC cell lines expressing HBx, and human and mouse HSCs were detected. The influences of miR-361 on the biological processes of HSCs were explored. The target of miR-361 and the effects of p65 on miR-361 were also verified and analyzed.
Results: Microarray analysis and quantitative real-time PCR (Q-PCR) indicated that miR-361 was decreased in HBV-relevant HCC tissues, HBx transgenic mice, HBx-transfected HepG2 cells, human and mice HSCs. Bio-informatics prediction and dual-luciferase reporter assay (DLRA) suggested that nuclear factor kappa B subunit p65 gene was a target of miR-361. Furthermore, this study showed that p65 expression was upregulated in the HBV-relevant HCC tissues, HBx transgenic mice, HBx-transfected HepG2 cells. MiR-361 upregulation also caused a reduction in p65 expression in both human and mice HSCs. In addition, p65 overexpression counteracted the effect of miR-361 in human and mice HSCs' biological processes. These findings reveal a latent mechanism underlying p65 modulation by miR-361 which is capable of initiating HSC growth and migration.
Conclusion: miR-361 is potentially functioning as a potent marker for HBV-relevant HCC development or liver fibrosis (LF) progression.
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| http://dx.doi.org/10.1016/j.cdev.2021.203711 | DOI Listing |
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