长非编码 RNA SUMO1P3 通过 Wnt/β-catenin 通路促进神经胶质瘤进展。

Long non-coding RNA SUMO1P3 promotes glioma progression via the Wnt/β-catenin pathway.

机构信息

Department of Neurosurgery, The First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi, P.R. China.

出版信息

Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9571-9580. doi: 10.26355/eurrev_202009_23044.

DOI:10.26355/eurrev_202009_23044

PMID:33015800

Abstract

OBJECTIVE

Long non-coding RNA SUMO1P3 has been reported to act as an oncogene in the tumorigenesis of several types of human malignancy. However, to the best of our knowledge, the exact biological functions and potential mechanism of lncRNA SUMO1P3 in glioma remains unknown. Therefore, the aim of this study was to investigate the potential role of SUMO1P3 in glioma and to explore the underlying mechanism.

PATIENTS AND METHODS

The present study examined SUMO1P3 expression in glioma tissues and cell lines using reverse transcription-quantitative polymerase chain reaction. Cell Counting Kit-8 (CCK-8) and transwell assays were used to examine the effects of SUMO1P3 on the proliferation and invasion of glioma cells, respectively. Furthermore, Western blot was used to detect the expression levels of proteins in the epithelial-mesenchymal transition (EMT) process.

RESULTS

The expression level of SUMO1P3 was higher in glioma tissues compared with corresponding adjacent normal tissues. In addition, a high expression level of SUMO1P3 was significantly associated with clinical progression and poor survival for patients with glioma. Furthermore, the knockdown of SUMO1P3 inhibited the proliferation, migration and invasion of U87 and U251 cells. In addition, the knockdown of SUMO1P3 inhibits glioma growth in vivo. Finally, the knockdown of SUMO1P3 inhibited the epithelial-mesenchymal transition and reduced the expression levels of active β-catenin, C-myc, and cyclin D1 in U87 and U251 cells. By contrast, the overexpression of SUMO1P3 promoted glioma cell proliferation, migration, and invasion.

CONCLUSIONS

SUMO1P3 promotes glioma cell proliferation, migration, and invasion, and may be involved in Wnt/β-catenin signaling.

摘要

目的

长链非编码 RNA SUMO1P3 已被报道在多种人类恶性肿瘤的发生中起癌基因作用。然而，据我们所知，lncRNA SUMO1P3 在神经胶质瘤中的确切生物学功能和潜在机制尚不清楚。因此，本研究旨在探讨 SUMO1P3 在神经胶质瘤中的潜在作用，并探讨其潜在机制。

患者和方法

本研究采用逆转录定量聚合酶链反应检测神经胶质瘤组织和细胞系中 SUMO1P3 的表达。细胞计数试剂盒-8（CCK-8）和 Transwell 分析分别用于检测 SUMO1P3 对神经胶质瘤细胞增殖和侵袭的影响。此外，Western blot 用于检测上皮-间充质转化（EMT）过程中蛋白的表达水平。

结果

与相应的癌旁正常组织相比，神经胶质瘤组织中 SUMO1P3 的表达水平更高。此外，SUMO1P3 高表达与神经胶质瘤患者的临床进展和不良预后显著相关。此外，SUMO1P3 的敲低抑制了 U87 和 U251 细胞的增殖、迁移和侵袭。此外，SUMO1P3 的敲低抑制了体内神经胶质瘤的生长。最后，SUMO1P3 的敲低抑制了上皮-间充质转化，并降低了 U87 和 U251 细胞中活性 β-catenin、C-myc 和 cyclin D1 的表达水平。相比之下，SUMO1P3 的过表达促进了神经胶质瘤细胞的增殖、迁移和侵袭。