Zekun Yu1, Jing Zhang1, Jun Han2. 1. Department of Neonatology, the First Hospital of Jilin University, No. 71, XinMin Street, Changchun, 130021, Jilin, China. 2. Department of Neonatology, the First Hospital of Jilin University, No. 71, XinMin Street, Changchun, 130021, Jilin, China. zitanzhan@163.com.
Abstract
BACKGROUND: Neuroblastoma is the commonest extracranial solid cancer for neonates. Long non-coding RNA cancer susceptibility 11 (CASC11) is corroborated as carcinogen in several tumors. But its role in neonatal neuroblastoma is poorly defined. METHODS: Expression levels of CASC11, miR-676-3p, and NOL4L mRNA were analyzed by qRT-PCR in cells and tissues. Kaplan-Meier analysis was used to measure and analyze the survival time of patients with high/low CASC11. Neonatal neuroblastoma cell proliferation was reflected through colony-formation assay and CCK-8. Transwell assay was designed for detection of migratory and invasive capacities of neonatal neuroblastoma cells. Wound-healing assay was used for monitoring neuroblastoma cell migration. RNA pull-down, luciferase reporter, and RIP assays were utilized to identify the relationship between CASC11, miR-676-3p, and NOL4L on the basis of bioinformatics tools. RESULTS: Highly expressed CASC11 was observed in neonatal neuroblastoma tissues and cells. High level of CASC11 indicated unsatisfactory survival of neonatal neuroblastoma patients. CASC11 depletion inhibited cell proliferation and invasiveness. CASC11 was a molecular sponge to release NOL4L from miR-676-3p inhibition in tumor cells. Upregulation of NOL4L abated the suppressed cell proliferation and invasiveness due to CASC11 downregulation. CONCLUSION: CASC11 sequestered miR-676-3p from NOL4L to facilitate neonatal neuroblastoma progression, hinting a CASC11-mediated therapeutic target for neonatal neuroblastoma.
BACKGROUND:Neuroblastoma is the commonest extracranial solid cancer for neonates. Long non-coding RNA cancer susceptibility 11 (CASC11) is corroborated as carcinogen in several tumors. But its role in neonatal neuroblastoma is poorly defined. METHODS: Expression levels of CASC11, miR-676-3p, and NOL4L mRNA were analyzed by qRT-PCR in cells and tissues. Kaplan-Meier analysis was used to measure and analyze the survival time of patients with high/low CASC11. Neonatal neuroblastoma cell proliferation was reflected through colony-formation assay and CCK-8. Transwell assay was designed for detection of migratory and invasive capacities of neonatal neuroblastoma cells. Wound-healing assay was used for monitoring neuroblastoma cell migration. RNA pull-down, luciferase reporter, and RIP assays were utilized to identify the relationship between CASC11, miR-676-3p, and NOL4L on the basis of bioinformatics tools. RESULTS: Highly expressed CASC11 was observed in neonatal neuroblastoma tissues and cells. High level of CASC11 indicated unsatisfactory survival of neonatal neuroblastomapatients. CASC11 depletion inhibited cell proliferation and invasiveness. CASC11 was a molecular sponge to release NOL4L from miR-676-3p inhibition in tumor cells. Upregulation of NOL4L abated the suppressed cell proliferation and invasiveness due to CASC11 downregulation. CONCLUSION:CASC11 sequestered miR-676-3p from NOL4L to facilitate neonatal neuroblastoma progression, hinting a CASC11-mediated therapeutic target for neonatal neuroblastoma.