MicroRNA-326 inhibits cell proliferative capacity and invasiveness through inhibiting the expression of ETS1 in nasopharyngeal carcinoma.

OBJECTIVE: This study aims to detect microRNA-326 expression in nasopharyngeal carcinoma (NPC) tissues and cell lines and to explore the potential mechanism of microRNA-326 inhibiting the proliferative capacity and invasiveness of NPC cells. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine microRNA-326 expression in 40 cases of NPC tissue samples and cell lines. Meanwhile, microRNA-326 mimics were transfected into NPC cells to up-regulate microRNA-326 level. Next, the influence of microRNA-326 mimics on the proliferation and invasiveness of NPC cells was observed by Cell Counting Kit-8 (CCK-8) assay and transwell assay, respectively. Bioinformatics analysis was applied to search for target genes which may have direct effects on microRNA-326. An EST1 luciferase reporter vector containing microRNA-326 binding site was constructed and the binding relation between ETS1 and microRNA-326 was detected by Dual-Luciferase reporting assay. Lastly, the underlying mechanism of microRNA-326 and ETS1 in NPC was further verified via cell reverse experiments. RESULTS: Compared with control group, microRNA-326 expression was found remarkably decreased both in NPC tissue specimens and cell lines. The low expression of microRNA-326 could predict poor prognosis of patients with NPC. In vitro cell experiments revealed that overexpression of microRNA-326 remarkably inhibited the proliferative capacity and invasiveness of NPC cells. Bioinformatics analysis and Dual-Luciferase assay results suggested that microRNA-326 may bind to ETS1. Cell reverse assay indicated that inhibiting ETS1 expression partially reversed the changes in cell biological behavior induced by the down-regulation of microRNA-326 in CNE1 and 5-8F cell lines. CONCLUSIONS: Overexpression of microRNA-326 in NPC cells could remarkably inhibit the proliferative capacity and invasiveness of NPC cells. In addition, microRNA-326 may participate in the development of NPC by inhibiting ETS1 expression.

The long non-coding RNA AK001796 contributes to poor prognosis and tumor progression in hepatocellular carcinoma.

OBJECTIVE: Increasing studies have indicated the important functions of long non-coding RNAs (lncRNAs) in tumorigenesis and progression including hepatocellular carcinoma (HCC). The study aims to explore the role of long non-coding RNA AK001796 in HCC progression. PATIENTS AND METHODS: Quantitative Real-time polymerase chain reaction (QRT-PCR) analysis was performed to examine the lncRNA AK001796 expression in 73 cases of human HCC tissue samples and matched adjacent normal tissues. Besides, the relationship between lncRNA AK001796 expression and clinicopathologic characteristics was analyzed. Overall survival (OS) curves of patients were constructed by the Kaplan-Meier methods. Multivariate Cox regression analysis was used to evaluate independent risk factors affecting HCC prognosis. Cell proliferation and invasion abilities are analyzed by cell counting kit-8 (CCK-8) and transwell invasion assays. RESULTS: We showed that the lncRNA AK001796 expression was significantly up-regulated in HCC tissues and cell lines, compared to their controls, respectively. Higher lncRNA AK001796 expression closely correlated with tumor size (p<0.05), TNM stage (p<0.05) and the poor overall survival (OS) rate of HCC patients (p<0.05). Besides, multivariate Cox regression analysis found that lncRNA AK001796 expression was identified as an independent risk factor for HCC prognosis. In vitro, we showed that lncRNA AK001796 knockdown markedly suppressed cell proliferation and cell invasion abilities. CONCLUSIONS: Our results suggested that lncRNA AK001796 acts as a predictor of HCC prognosis and may provide an important clinical value for HCC treatment.