miR-135a inhibits the proliferation of HBV-infected hepatocellular carcinoma cells by targeting HOXA10.

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 miR-135a and HOXA10 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 miR-135a. Overexpression of miR-135a was used to measure the roles of miR-135a in the proliferation, invasion, and apoptosis of HCC cells. A dual luciferase experiment was performed to assess the relationship between HOXA10 and miR-135a. Western blot was applied to observe the protein levels of p-p38, p-ERK, and p-JNK. Results: The expression levels of miR-135a were significantly decreased in HCC tissues and cells. Overexpression of miR-135a inhibited the proliferation and invasion but promoted the apoptosis of HCC cells. Importantly, our results confirmed that HOXA10 was a direct target of miR-135a. Under HBV infection, silencing of HOXA10 significantly blocked the proliferation and invasion and promoted the apoptosis of HCC cells. In addition, miR-135a/HOXA10 regulated the expressions of p-p38, p-ERK, and p-JNK through the miR-135a/HOXA10 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 miR-135a/HOXA10 pathway. These findings provide a theoretical basis for improving the treatment of HBV-infected HCC patients.