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Original Research

MicroRNA-339 inhibits human hepatocellular carcinoma proliferation and invasion via targeting ZNF689

, , , , &
Pages 435-445 | Published online: 22 Jan 2019
 

Abstract

Background

Hepatocellular carcinoma (HCC) is the second leading cause of cancer mortality worldwide, however, the prognosis for HCC remains unsatisfactory. This study aimed to explore the role of miR-339-5p in HCC.

Methods

We first used quantitative real-time PCR to examine the level of miR-339-5p in HCC tissues. Then we further adopted Western blotting assay, CCK8, cell invasion assays, apoptosis detection assay, and luciferase assay to analyze how it mediate the development of HCC.

Results

We found that miR-339 is significantly decreased in primary HCC tissues. Overexpression of miR-339 in HCC cells remarkably suppressed proliferation and invasion and induced apoptosis. However, silencing miR-339 in HCC cells promoted proliferation and invasion, and reduced apoptosis. Moreover, we demonstrated that ZNF689 is a target of miR-339 and there is a negative correlation between miR-339 and ZNF689 expression in the HCC tissues. Overexpression of ZNF689 in miR-339-overexpressing HCC cells partially antagonized the inhibitory effects of miR-339.

Conclusion

Our study revealed that miR-339 inhibits HCC growth through targeting oncoprotein ZNF689 and restoration of miR-339 might be feasible therapeutic strategy for HCC treatment.

Disclosure

The authors report no conflicts of interest in this work.

Supplementary materials

Table S1 Primer sequences used in qPCR assay

Table S2 Correlation between miR-339 levels and the 20 HCC patients’ clinicopathological parameters

Figure S1 Overexpression of ZNF689 antagonizes the apoptotic effect induced by miR-339 in HCCLM3 cells.

Note: After ZNF689 overexpression plasmid was co-transfected with miR-339 mimic into HCCLM3 cells, the protein expression of cleaved-PARP, cleaved-caspase3 and cleaved-caspase8 was detected at 72 h by using Western blotting.
Figure S1 Overexpression of ZNF689 antagonizes the apoptotic effect induced by miR-339 in HCCLM3 cells.