inhibits the proliferation of HBV-infected hepatocellular carcinoma cells by targeting .

BACKGROUND

The incidence of hepatocellular carcinoma (HCC) in patients with hepatitis B virus (HBV) is extremely high. MicroRNAs (miRNAs) are a type of endogenous non-coding small RNA with novel molecular therapeutic mechanisms that plays an important role in the occurrence and development of cancers. This study aimed to explore the regulation mechanism of and in the proliferation, invasion, and apoptosis of HCC cells.

METHODS

Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis was used to detect the expression level of . Overexpression of was used to measure the roles of in the proliferation, invasion, and apoptosis of HCC cells. A dual luciferase experiment was performed to assess the relationship between and . Western blot was applied to observe the protein levels of , , and .

RESULTS

The expression levels of were significantly decreased in HCC tissues and cells. Overexpression of inhibited the proliferation and invasion but promoted the apoptosis of HCC cells. Importantly, our results confirmed that was a direct target of . Under HBV infection, silencing of significantly blocked the proliferation and invasion and promoted the apoptosis of HCC cells. In addition, / regulated the expressions of p-p38, p-ERK, and p-JNK through the / axis, thereby inhibiting the activation of the MAPK pathway.

CONCLUSIONS

HBV promoted the proliferation and invasion, and inhibited the apoptosis of HCC cells by regulating the / pathway. These findings provide a theoretical basis for improving the treatment of HBV-infected HCC patients.