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OBJECTIVE: To investigate whether lncRNA H19 can regulate NF1 expression through competitive binding to microRNA- 107, thereby participating in the occurrence and development of non-small cell lung cancer (NSCLC). PATIENTS AND METHODS: Expression levels of H19 and NF1 in NSCLC tissues, paracancerous tissues and NSCLC cell lines were detected by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). The binding condition of microRNA-107, H19 and NF1 was detected by dual-luciferase reporter gene assay. Corresponding lentiviruses of H19 were constructed. The regulatory effects of H19 on proliferative and migratory abilities of A549 cells were detected by cell counting kit-8 (CCK-8) and transwell assay, respectively. Rescue experiments were conducted to explore the regulatory interaction between H19 and microRNA-107 in A549 cells. RESULTS: H19 and NF1 were highly expressed in NSCLC tissues and NSCLC cell lines (A549 and HCC823) than those of controls. Overexpressed H19 increased proliferative and migratory abilities of A549 cells. Dual-luciferase reporter gene assay demonstrated that H19 regulates NF1 expression through competitive binding to microRNA-107, thereafter participating in NSCLC development. CONCLUSIONS: H19 is highly expressed in NSCLC, which promotes NSCLC development by regulating NF1 via competitive binding to microRNA- 107. [ABSTRACT FROM AUTHOR]

Epstein-Barr virus (EBV) is a well-documented aetiological factor for multiple sclerosis (MS). EBV encodes at least 44 microRNAs (miRNAs) that are readily detectable in the circulation of human. Previous studies have demonstrated that EBV-encoded miRNAs regulate host immune response and may serve as biomarkers for EBV-associated diseases. However, the roles of EBV miRNAs in MS are still unknown. To fill the gap, we conducted a comprehensive profiling of 44 mature EBV miRNAs in 30 relapsing-remitting MS (RRMS) patients at relapse and 30 matched healthy controls. Expression levels of ebv-miR-BHRF1-2-5p and ebv-miR-BHRF1-3 were elevated significantly in the circulation and correlated positively with the expanded disability status scale (EDSS) scores of MS patients. Receiver operating characteristic (ROC) analyses confirmed that the expression of these two miRNAs distinguished MS patients clearly from healthy controls. Luciferase assays revealed that ebv-miR-BHRF1-2-5p may directly target MALT1 (mucosa-associated lymphoid tissue lymphoma transport protein 1), a key regulator of immune homeostasis. In conclusion, we described the expression of EBV miRNAs in MS and preliminarily validated the potential target genes of significantly altered EBV miRNAs. The findings may pave the way for prospective study about the pathogenesis of MS. [ABSTRACT FROM AUTHOR]