Abstract

This study aimed at exploring the expression and prognostic values of a novel long noncoding RNA RUSC1-AS-N in hepatocellular carcinoma (HCC), and to investigate the biological roles of RUSC1-AS-N in HCC cells. RUSC1-AS-N expression in public available microarray data was analyzed. The expression of RUSC1-AS-N in our cohort containing 66 HCC tissues and paired adjacent non-cancerous hepatic tissues was measured by qRT-PCR. The correlation between RUSC1-AS-N expression and clinicopathological characteristics was evaluated by Pearson χ2-test. The prognostic value of RUSC1-AS-N was analyzed by Kaplan-Meier survival analysis. The biological roles of RUSC1-AS-N on HCC cell viability were evaluated by Glo cell viability assays and Ethynyl deoxyuridine incorporation assays. The effects of RUSC1-AS-N on HCC cell cycle were evaluated by fluorescence-activated cell sorting (FACS) analyses of propidium-iodide (PI) stained cells. The effects of RUSC1-AS-N on HCC cell apoptosis were evaluated by TdT-mediated dUTP nick end-labeling (TUNEL) assays. RUSC1-AS-N is upregulated in HCC tissues and associated with poor prognosis of HCC patients from GSE54238 and GSE40144. In our cohort, we further confirmed the upregulation of RUSC1-AS-N in HCC tissues. High expression of RUSC1-AS-N associates with large tumor size, vein invasion, encapsulation incompletion, advanced BCLC stage, and poor recurrence-free survival and overall survival. Functional assays revealed that RUSC1-AS-N knockdown markedly decreases cell viability, induces cell-cycle arrest and apoptosis of HCC cells. RUSC1-AS-N is upregulated and acts as an oncogene in HCC. RUSC1-AS-N may be a promising prognostic biomarker and therapeutic target for HCC.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.