Luo Zhengxiang, Pan Junchen, Ding Yi, Zhang Yan-Song, Zeng Yanjun
Department of Neurosurgery, Nanjing Brian Hospital Affiliated to Nanjing Medical University, Nanjing, China.
Department of Neurosurgery, Nanjing Benq Hospital, Nanjing, Jiangsu, China.
Arch Med Sci. 2018 Oct;14(6):1308-1320. doi: 10.5114/aoms.2018.79004. Epub 2018 Oct 23.
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.
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.
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.
These data suggest an important role of UBE2CP3-001 in glioma and indicate its potential application in anti-glioma therapy.
胶质瘤是人类大脑中最常见的原发性肿瘤。最近的研究发现了一类长链非编码RNA,称为lncRNAs,据报道它们参与调节包括胶质瘤在内的各种疾病的发展。在我们之前的研究中,我们发现lncRNA UBE2CP3 - 001在胶质瘤中过表达,但在正常组织中未过表达。然而,UBE2CP3 - 001在胶质瘤中的分子功能在很大程度上尚不清楚。
通过实时RT - PCR检测UBE2CP3 - 001在U87细胞、胶质瘤组织和正常脑组织中的存在情况。在下调UBE2CP3 - 001后,使用细胞伤口愈合试验分析U87细胞的迁移能力。还使用CCK8试验分析UBE2CP3 - 001敲低后U87细胞的存活率。使用动物实验进一步分析用UBE2CP3 - 001 shRNA转染的异种移植肿瘤的肿瘤重量。通过蛋白质免疫印迹法测定MMP - 9和TRAF3IP2的表达水平。
我们的数据表明,UBE2CP3 - 001在大多数胶质瘤组织中过表达(<0.01)。下调UBE2CP3 - 001可抑制U87细胞的迁移(<0.01)和侵袭性(<0.01)。下调U87细胞中的UBE2CP3 - 001也抑制了细胞增殖(<0.01)并促进了细胞凋亡(<0.01)。此外,研究证实敲低UBE2CP3 - 001可延缓U87异种移植肿瘤的生长(<0.01)。蛋白质免疫印迹分析表明,敲低UBE2CP3 - 001可有效抑制U87胶质瘤细胞中MMP - 9(<0.01)和TRAF3IP2(<0.01)的表达。
这些数据表明UBE2CP3 - 001在胶质瘤中起重要作用,并表明其在抗胶质瘤治疗中的潜在应用。