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Overexpression of miR-1283 Inhibits Cell Proliferation and Invasion of Glioma Cells by Targeting ATF4

It is well known that activating transcription factor 4 (ATF4) expression is closely associated with progression of many cancers. We found that miR-1283 could directly target ATF4. However, the precise mechanisms of miR-1283 in glioma have not been well clarified. Our study aimed to explore the inte...

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Detalles Bibliográficos
Autores principales: Chen, Hao, Zhang, Yi, Su, Hai, Shi, Hui, Xiong, Qijiang, Su, Zulu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cognizant Communication Corporation 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7848429/
https://www.ncbi.nlm.nih.gov/pubmed/29716673
http://dx.doi.org/10.3727/096504018X15251282086836
Descripción
Sumario:It is well known that activating transcription factor 4 (ATF4) expression is closely associated with progression of many cancers. We found that miR-1283 could directly target ATF4. However, the precise mechanisms of miR-1283 in glioma have not been well clarified. Our study aimed to explore the interaction between ATF4 and miR-1283 in glioma. In this study, we found that the level of miR-1283 was dramatically decreased in glioma tissues and cell lines, the expression of ATF4 was significantly increased, and the low level of miR-1283 was closely associated with high expression of ATF4 in glioma tissues. Moreover, introduction of miR-1283 significantly inhibited proliferation and invasion of glioma cells. However, knockdown of miR-1283 promoted the proliferation and invasion in glioma cells. Bioinformatics analysis predicted that the ATF4 was a potential target gene of miR-1283. Luciferase reporter assay demonstrated that miR-1283 could directly target ATF4. In addition, knockdown of ATF4 had similar effects with miR-1283 overexpression on glioma cells. Upregulation of ATF4 in glioma cells partially reversed the inhibitory effects of miR-1283 mimic. Overexpression of miR-1283 inhibited cell proliferation and invasion of glioma cells by directly downregulating ATF4 expression.