miR-29a-5p regulates the malignant biological process of liver cancer cells through ARID2 regulation of EMT

Background. Liver cancer, the vast majority of cases being hepatocellular carcinoma (HCC), is now the most malignant tumor in the world. Recurrence and metastasis remain the major obstacles on the way to the successful treatment of HCC. In recent years, the vital function of microRNAs (miRNAs) in human health and disease have been demonstrated. Large amounts of evidence demonstrate that miRNAs play an important role in the occurrence and progression of HCC. Objectives. To find new targets for improving the early diagnosis, treatment and clinical prognosis of liver cancer. Materials and methods. We used quantitative reverse transcription-polymerase chain reaction (qRT-PCR) to analyze the expression of miR-29a-5p. A cell counting kit-8 (CCK-8) assay was used to measure the proliferation of liver cancer cells. Wound healing and transwell assays were used to detect migration and invasion in vitro. Western blot was used to detect the expression of the related protein. Results. The miR-29a-5p was identified as a tumor-related miRNA. It is upregulated in HCC. The overexpression of miR-29a-5p contributes to the proliferation, invasion and metastasis of HCC cells. Furthermore, the downregulation of miR-29a-5p inhibited the growth, migration and invasion of HCC cells in vitro. Subsequently, we used bioinformatics methods to predict that AT-rich interaction domain 2 (ARID2) is the down-stream target gene of miR-29a-5p. The downregulation of ARID2 could reverse the tumor suppressive effect caused by the knockdown of miR-29a-5p. Similarly, the epithelial-mesenchymal transition (EMT)-related protein epithelial marker E-cadherin expression increased and the mesenchymal marker Vimentin decreased when we downregulated the expression of miR-29a-5p. Interestingly, the knockdown of ARID2 could reverse this phenomenon. Conclusions. Our study demonstrated that miRNA-29a-5p was overexpressed in HCC cells. It promotes the progression of HCC by targeting ARID2 in an EMT manner.