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A Novel Circular RNA, circ_0005394, Predicts Unfavorable Prognosis and Contributes to Hepatocellular Carcinoma Progression by Regulating miR-507/E2F3 and miR-515-5p/CXCL6 Signaling Pathways.

ABSTRACT: ObjectiveCircular RNAs (circRNAs) play a key role in cancer development and progression. Previously, circ_0005394 was found to be highly expressed in hepatocellular carcinoma (HCC) screened by circRNA microarray. However, the research with regard to the functions and mechanisms of circ_0005394 in HCC remains unknown.Materials and MethodsThe expression of circ_0005394 in HCC was measured by qRT-PCR. The clinical relevance was evaluated by Fisher’s exact test, Kaplan–Meier curves, and Cox regression model. Gain/loss-of function assays were performed to elucidate the functions of circ_0005394 in Huh-7 and HepG2 cells. Dual-luciferase reporter assay was applied to reveal the mechanism of circ_0005394.Resultscirc_0005394 expression was higher in HCC tissues and cells than noncancerous samples and normal cell line, respectively. High expression of circ_0005394 was associated with larger tumor size, more advanced TNM stages, and poorer overall survival for the patients with HCC. Gain/loss-of function assays demonstrated its oncogenic role in cell growth, apoptosis, migration, and invasion. Mechanistically, miR-507 and miR-515-5p could be sponged by circ_0005394. Furthermore, E2F Transcription Factor 3 (E2F3) and C-X-C motif chemokine ligand 6 (CXCL6) were confirmed as the target of miR-507 and miR-515-5p, respectively. Rescue assay indicated that circ_0005394 facilitated HCC growth and invasion by regulating miR-507/E2F3 and miR-515-5p/CXCL6 signaling pathways.ConclusionThis study uncovered an important role of circ_0005394 in regulating HCC progression, providing a novel perspective for clarifying its pathogenesis.

SUBMITTER: Sun C

PROVIDER: S-EPMC7334013 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Project description:Dysregulation of circular RNAs (circRNAs) has recently been found to play an important role in the progression and development of cancers such as non-small cell lung cancer (NSCLC). Yet the functions of many circRNAs in NSCLC remain unclear. In this study, the circRNA expression profiles in NSCLC tumor tissues and adjacent non-tumorous tissues were detected by high-throughput sequencing. Bioinformatics analyses, the dual-luciferase reporter system, fluorescence in situ hybridization (FISH) and miRNA/mRNA high-throughput sequencing were used to identify circ-EPB41 and its downstream target. The subcutaneous tumor/caudal vein transfer mouse model was used for tumor growth and invasion analysis. The results show that the circ-EPB41 was upregulated in NSCLC tissues and cell lines. Increased circ-EPB41 expression in NSCLC was significantly correlated with malignant characteristics, and positive to post-surgical overall survival of NSCLC patients. Reduced circ-EPB41 expression in NSCLC decreased cell proliferation and invasion in both in vitro and in vivo experiments. The miRNA/mRNA high-throughput sequencing suggested that downregulation of circ-EPB41 promoted microRNA (miR)-486-3p and suppressed eukaryotic translation initiation factor 5A (eIF5A) expression. Luciferase reporter experiments confirmed that miR-486-3p/eIF5A were downstream targets of circ-EPB41. In addition, we also found that downregulation of circ-EPB41 suppressed self-renewal and decreased expression of stemness markers SOX2, OCT-4, Nanog and CD133 by sponging miR-486-3p to enhance eIF5A expression. Taken togeter, these data revealed the important role of circ-EPB41 in regulating NSCLC cell invasion and proliferation by modifying miR-486-3p/eIF5A axis-mediated stemness. We believe our study provides a novel perspective regarding the role of circRNAs in NSCLC progression. Supplementary Information The online version contains supplementary material available at 10.1186/s12935-022-02618-7.

Dataset Information

A Novel Circular RNA, circ_0005394, Predicts Unfavorable Prognosis and Contributes to Hepatocellular Carcinoma Progression by Regulating miR-507/E2F3 and miR-515-5p/CXCL6 Signaling Pathways.

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