Abstract
The long noncoding RNA (lncRNA) antisense noncoding RNA in the INK4 locus (ANRIL) expression is upregulated in hepatocellular carcinoma (HCC) tissues, and decreased ANRIL expression inhibits cell proliferation, metastasis, and invasion and induces apoptosis in HCC cells. However, the molecular mechanism by which ANRIL is involved in HCC tumorigenesis is unclear. In this study, ANRIL was found to be a significantly upregulated lncRNA in HCC and was associated with the metastasis and poor prognosis of HCC. p53 plays an important role in the mechanism of carcinogenesis. Therefore, we hypothesized that ANRIL plays a biological role by regulating the p53 signaling pathway. To comprehensively evaluate the biological function of ANRIL, bioinformatics analysis, quantitative real-time polymerase chain reaction, Western blotting, wound healing, Transwell, cell colonization assay, cell counting kit-8, reactive oxygen species, JC-1, EdU, and terminal deoxynucleotidyl transferase-mediated dUTP Nick end labeling were performed. The results showed that the knockdown of ANRIL inhibited HCC cell viability, colony forming ability, functions such as metastasis and invasion, and epithelial–mesenchymal transition. Meanwhile, the knockdown of ANRIL also resulted in the decreased expression of the p53 protein. All these effects are tightly intertwined with the regulation of the p53 signaling pathway. Thus, ANRIL may contribute to the development of new drugs for the treatment of human HCC.
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