Astrocyte elevated gene-1 serves as a target of miR542 to promote glioblastoma proliferation and invasion.
10.1097/CM9.0000000000001072
- Author:
Chong LI
1
;
Hai-Long LIU
1
;
Yu-Mei ZHOU
2
;
Yan-Chun SHI
2
;
Zhi-Bin ZHANG
1
;
Ling CHEN
1
;
Shi-Yu FENG
1
Author Information
1. Department of Neurosurgery, The First Medical Center of Chinese People's Liberation Army General Hospital, Beijing 100853, China.
2. Beijing University of Chinese Medicine, Beijing 100029, China.
- Publication Type:Journal Article
- MeSH:
Astrocytes;
Cell Line, Tumor;
Cell Movement/genetics*;
Cell Proliferation/genetics*;
Epithelial-Mesenchymal Transition/genetics*;
Gene Expression Regulation, Neoplastic;
Glioblastoma/genetics*;
Humans;
MicroRNAs/genetics*;
Neoplasm Invasiveness/genetics*
- From:
Chinese Medical Journal
2020;133(20):2437-2443
- CountryChina
- Language:English
-
Abstract:
BACKGROUND:Epithelial to mesenchymal transition (EMT) is strongly linked with tumor invasion and metastasis, which performs a vital role in carcinogenesis and cancer progression. Emerging evidence suggests that microRNAs (miRNAs) expression are closely associated to EMT by regulating targeted genes. MiR542 has been found to be involved in the EMT program and bound up with various cancers. However, the functions of miR542 and its underlying mechanism in glioblastoma multiforme (GBM) remain largely unknown. In the current study, we investigated the effect of astrocyte elevated gene-1 (AEG-1) on U251 cells aggressiveness, proliferation, apoptosis, and cell cycle.
METHODS:The screening of targeted miRNAs was performed, as well as the functional roles and mechanisms of miR542 were explored.
RESULTS:MiR542 was selected as the target because of the most significantly differential expression and this high level of expression negatively correlated with cell migration and proliferation, which suggested that miR542 could be a novel tumor suppressor. Moreover, we confirmed that AEG-1 was a direct targeted gene of miR542 by luciferase activity assay, reverse transcription-polymerase chain reaction, and immunoblotting analysis. Furthermore, miR542 suppressed the expression of AEG-1, which upgraded the level of E-cadherin and degraded Vimentin expression contributing to retraining EMT.
CONCLUSION:The in vitro findings demonstrated that miR542 inhibited the migration and proliferation of U251 cells and suppressed EMT through targeting AEG-1, indicating that miR542 may be a potential anti-cancer target for GBM.
