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

Arch Med Sci

Biomechanics and Medical Information Institute, Beijing University of Technology, Beijing, China.

Published: October 2018

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. tumor weights from xenograft tumors transfected with UBE2CP3-001 shRNA were further analyzed using 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 ( < 0.01). Downregulation of UBE2CP3-001 could inhibit cell migration ( < 0.01) and invasiveness ( < 0.01) of U87 cells. Downregulation of UBE2CP3-001 in U87 cells also suppressed the cell proliferation ( < 0.01) and promoted apoptosis ( < 0.01). Furthermore, studies confirmed that knockdown of UBE2CP3-001 could retard the growth of U87 xenograft tumors ( < 0.01). Western blot analysis showed that knockdown of UBE2CP3-001 could effectively inhibit the expression of MMP-9 ( < 0.01) and TRAF3IP2 ( < 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6209712PMC
http://dx.doi.org/10.5114/aoms.2018.79004DOI Listing

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