LncRNA CRNDE promotes hepatocellular carcinoma cell proliferation, invasion, and migration through regulating miR-203/ BCAT1 axis. Journal of cellular physiology OBJECTIVE:To investigate the impact of long noncodingRNA (lncRNA) colorectal neoplasia differentially expressed (CRNDE) on hepatocellular cancer (HCC) cell propagation, invasion, and migration by mediating miR-203/ BCAT1 axis. METHODS:Microarray analysis was based on 25 pairs of HCC cancerous tissues and adjacent tissues. The expression levels of CRNDE, miR-203, and BCAT1 in HCC tissues were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). The liver cell line L-02 and HCC cell lines HepG2 and Huh-7 were utilized to assess the regulatory effects of CRNDE and miR-203 on HCC progression in vitro. Western blot was used to qualify BCAT1 protein expression level. Cell proliferation and apoptosis were evaluated using CCK-8 and flow cytometry analysis, whereas cell invasion and migration assay were performed by the Transwell assay. The relationship among CRNDE, miR-203, and BCAT1 was validated by dual luciferase assay. Tumor Xenograft study was established to verify the pathological effect of CRNDE on HCC development in vivo. RESULTS:The expression levels of the CRNDE and BCAT1 were upregulated in HCC tissues and cells, whereas miR-203 was downregulated in HCC. Knockdown of CRNDE or miR-203 overexpression would inhibit HCC cell propagation and metastasis, and induced cell apoptosis. Moreover, miR-203 was negatively correlated with CRNDE, the same as miR-203 with BCAT1. Dual luciferase assay showed that miR-203 was an inhibitory target of CRNDE, and BCAT1 was directly targeted by miR-203 as well. CONCLUSION:LncRNA CRNDE could enhance HCC tumorgenesis by sponging miR-203 and mediating BCAT1. LncRNA CRNDE might facilitate HCC cell propagation, invasiveness, and migration through regulating miR-203/ BCAT1 axis. 10.1002/jcp.27396

Downregulation of long noncoding RNA CRNDE suppresses drug resistance of liver cancer cells by increasing microRNA-33a expression and decreasing HMGA2 expression. Cell cycle (Georgetown, Tex.) At present, some researches have revealed the participation of long noncoding RNAs (lncRNAs) in liver cancer, but few of them have mentioned the role of CRNDE in drug resistance of liver cancer. Hence, this study is conducted to understand the role of CRNDE on liver cancer by regulating microRNA-33a (miR-33a) and high mobility group protein A2 (HMGA2) in liver cancer. First, drug-resistance model (HepG2 and BEL-7402) of human liver cancer cells was established. Then, CRNDE expression in drug-resistant cell lines (HepG2/adriamycin [ADM], BEL-7402/ADM) and parental cell lines (HepG2, BEL-7402) was detected. Furthermore, HepG2/ADM and BEL-7402/ADM cell lines with poor CRNDE expression or miR-33a overexpression was constructed. Next, drug-resistance index was calculated, and cell proliferation, apoptosis, migration, and invasion were detected, respectively. Then, the growth of tumor was observed in nude mice. Finally, the binding relationship between CRNDE and miR-33a and the targeting relationship between miR-33a and HMGA2 were verified. LncRNA CRNDE expressed highly in drug-resistant cells of liver cancer. Downregulated CRNDE and upregulated miR-33a-inhibited cells drug-resistance and promoted their apoptosis in liver cancer drug-resistant cells. CRNDE adsorbing and inhibiting miR-33a to promote HMGA2 in liver cancer drug-resistant cells by acting as a ceRNA. Silencing CRNDE or up-regulating miR-33a inhibited tumor growth of liver cancer . Our study provides evidence that downregulated CRNDE could upregulate miR-33a and inhibit HMGA2 expression, thus significantly promotes apoptosis of liver cancer cells and inhibiting its proliferation, migration, invasion and drug resistance. 10.1080/15384101.2019.1652035