miR-548b-3p Regulates Proliferation, Apoptosis, and Mitochondrial Function by Targeting CIP2A in Hepatocellular Carcinoma

Abstract EN

The roles of miR-548b-3p in the progression of hepatocellular carcinoma (HCC) remain undiscovered.

This study aims to explore the roles and mechanisms of miR-548b-3p in HCC.

Using TCGA database, we found that miR-548b-3p expression was lower in HCC compared to the normal tissues, which was further confirmed by RT-qPCR of 20 cases of surgically resected HCC and corresponding normal tissues.

miR-548b-3p mimic and inhibitor were transfected into Huh7 and SK-Hep-1 cells, respectively.

MTT, colony formation, and cell cycle assays showed that miR-548b-3p mimic suppressed cell growth and G1/S cell cycle transition.

In contrast, miR-548b-3p inhibitor facilitated cell growth and cell cycle transition.

miR-548b-3p mimic also increased cisplatin sensitivity by upregulating apoptosis rate.

JC-1 staining showed that miR-548b-3p mimic downregulated mitochondrial membrane potential, while miR-548b-3p inhibitor showed the opposite effects in SK-Hep-1 cells.

Using prediction software, we found that CIP2A was on the target list of miR-548b-3p.

miR-548b-3p mimic downregulated CIP2A and its downstream target protein c-Myc.

Luciferase reporter assay demonstrated that CIP2A was as a direct target of miR-548b-3p.

CIP2A depletion partly reduced the effect of miR-548b-3p mimic/inhibitor on c-Myc.

CIP2A depletion also reduced the effect of miR-548b-3p mimic/inhibitor on proliferation.

In conclusion, our data demonstrated that miR-548b-3p was downregulated in HCC.

miR-548b-3p regulates proliferation, apoptosis and mitochondrial function by targeting CIP2A in HCC.