The role of AURKA/miR‐199b‐3p in hepatocellular carcinoma cells

BACKGROUND: Previous studies proved that AURKA functions as an oncogene in several cancers. This article aimed to probe the miRNA‐induced regulatory mechanism of AURKA in hepatocellular carcinoma (HCC). METHODS: Differentially expressed genes in TCGA‐LIHC dataset were screened by bioinformatics methods. Levels of miR‐199b‐3p and AURKA mRNA were examined by qRT‐PCR. Western blot was utilized to evaluate protein levels of AURKA, p‐AKT, and AKT. Dual‐luciferase assay was introduced to explore their interaction. MTT, colony formation, scratch healing, transwell, and flow cytometry assays were introduced into cell proliferation, migration, invasion, and apoptosis assessment. The impact of miR‐199b‐3p/AURKA axis on HCC tumor growth was determined in a tumor xenograft model. RESULTS: We found that AURKA was highly expressed in HCC and was coupled to poor prognosis of HCC. As manifested by cellular assays, compared to the normal cells HL‐7702, AURKA presented notably high expression in HCC cell lines. Overexpressed AURKA evidently impelled the proliferation, colony formation, migration, and invasion of HCC cells while suppressing apoptosis. The regulatory gene upstream of AURKA was predicted to be miR‐199b‐3p by bioinformatics method, and there was a markedly negative correlation between the two. Overexpressed miR‐199b‐3p constrained HCC cell proliferation, migration, and invasion while fostering apoptosis, which could be counteracted by upregulating AURKA. MiR‐199b‐3p repressed the tumor growth in vivo by targeting AURKA and affected PI3K/AKT signaling pathway. CONCLUSION: To summarize, this study implied the regulatory mechanism of miR‐199b‐3p/AURKA axis in HCC, and supplied optional therapeutic targets for HCC patients.