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The function and clinical relevance of lncRNA UBE2CP3-001 in human gliomas

INTRODUCTION: Gliomas are the most frequent primary tumors in the human brain. Recent studies have identified a class of long noncoding RNAs, named lncRNAs, which were reported to participate in regulating the development of various diseases, including gliomas. In our previous studies, we found that...

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Detalles Bibliográficos
Autores principales: Luo, Zhengxiang, Pan, Junchen, Ding, Yi, Zhang, Yan-Song, Zeng, Yanjun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6209712/
https://www.ncbi.nlm.nih.gov/pubmed/30393485
http://dx.doi.org/10.5114/aoms.2018.79004
Descripción
Sumario:INTRODUCTION: Gliomas are the most frequent primary tumors in the human brain. Recent studies have identified a class of long noncoding RNAs, named lncRNAs, which were reported to participate in regulating the development of various diseases, including gliomas. In our previous studies, we found that lncRNA UBE2CP3-001 was overexpressed in gliomas but not in normal tissue. However, the molecular functions of UBE2CP3-001 in glioma are largely unknown. MATERIAL AND METHODS: The presence of UBE2CP3-001 in U87 cells, glioma tissues and normal brain tissues was detected by real-time RT-PCR. The ability of U87 cells to migrate was analyzed using a cellular wound healing assay after downregulation of UBE2CP3-001. The survival rate of U87 cells after UBE2CP3-001 knockdown was also analyzed using the CCK8 assay. In vivo tumor weights from xenograft tumors transfected with UBE2CP3-001 shRNA were further analyzed using in vivo animal experiments. The expression levels of MMP-9 and TRAF3IP2 were determined by Western blot. RESULTS: Our data showed that UBE2CP3-001 was overexpressed in most glioma tissues (p < 0.01). Downregulation of UBE2CP3-001 could inhibit cell migration (p < 0.01) and invasiveness (p < 0.01) of U87 cells. Downregulation of UBE2CP3-001 in U87 cells also suppressed the cell proliferation (p < 0.01) and promoted apoptosis (p < 0.01). Furthermore, in vivo studies confirmed that knockdown of UBE2CP3-001 could retard the growth of U87 xenograft tumors (p < 0.01). Western blot analysis showed that knockdown of UBE2CP3-001 could effectively inhibit the expression of MMP-9 (p < 0.01) and TRAF3IP2 (p < 0.01) in U87 glioma cells. CONCLUSIONS: These data suggest an important role of UBE2CP3-001 in glioma and indicate its potential application in anti-glioma therapy.