Knockdown of long noncoding RNA colorectal neoplasia differentially expressed inhibits hepatocellular carcinoma progression by mediating the expression of nuclear autoantigenic sperm protein

Abstract

Long noncoding RNAs (lncRNAs) play critical roles in the tumorigenesis and progression of hepatocellular carcinoma (HCC). As the most common malignant cancer type in humans, HCC poses a great threat to human health. However, the function of lncRNA colorectal neoplasia differentially expressed (CRNDE) in HCC has not been extensively studied. The chief aim of the present study was to reveal the potential role of CRNDE in HCC. Expression levels of CRNDE in HCC tissues and cell lines were detected by reverse transcription-quantitative (RT-q) PCR, and Cell Counting kit 8, wound-healing and Transwell assays were used to evaluate the influences of CRNDE on in vitro cellular proliferation, migration and invasiveness, respectively. The interaction between CRNDE and microRNA (miR)-29c-3p was determined by dual-luciferase reporter assay, and rescue experiments were conducted to evaluate the interactive relationships between CRNDE and miR-29c-3p or nuclear autoantigenic sperm protein (NASP). CRNDE was found to be upregulated in HCC tissues and cells, and to be positively associated with the poor prognosis of patients with HCC. Furthermore, CRNDE-knockdown suppressed cell proliferation, migration and invasion abilities. Bioinformatics and RT-qPCR analysis indicated miR-29c-3p as a potential target of CRNDE. In line with previous reports, as a tumor suppressor, downregulated expression of miR-29c-3p was observed in HCC. In addition, the present study revealed that miR-29c-3p directly targeted NASP. NASP expression was markedly elevated following transfection with an miR-29c-3p inhibitor, while knocking down CRNDE inhibited NASP expression. Moreover, the effects of CRNDE and NASP on HCC cells were reversed by miR-29c-3p. Collectively, the results of the present study revealed that CRNDE was upregulated and exerted an oncogenic role in HCC by targeting miR-29c-3p, and that the upregulation of CRNDE also promoted NASP expression. These findings indicate a novel role for CRNDE in the progression of HCC.