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CircZNF609/miR‐134‐5p/BTG‐2 axis regulates proliferation and migration of glioma cell
Author(s) -
Tong Hui,
Zhao Kai,
Wang Jiangjie,
Xu Hui,
Xiao Jianqi
Publication year - 2020
Publication title -
journal of pharmacy and pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 118
eISSN - 2042-7158
pISSN - 0022-3573
DOI - 10.1111/jphp.13188
Subject(s) - glioma , cell growth , microrna , downregulation and upregulation , cell migration , cell , competing endogenous rna , microbiology and biotechnology , u87 , gene knockdown , biology , cancer research , chemistry , cell culture , gene , long non coding rna , genetics
Objectives MicroRNAs are abundant in eukaryotic cells and play key roles in cancers. Circular RNAs (CircRNAs) served as the competing endogenous RNAs (ceRNAs) in mediating multiple cell processes. This study aims to define the role of CircRNA CircZNF609/miR‐134‐5p in glioma as well as the underlying regulating mechanism. Methods Relative expression of miR‐134‐5p, CircZNF609 and BTG‐2 mRNA was determined by quantitative real‐time PCR. Cell proliferation was analysed by CCK‐8 assay. Cell migration was assessed by cell wound scratch assay. The direct regulatory of miR‐134‐5p on BTG‐2 and CircZNF609 was verified by luciferase report gene assay. Key findings MiR‐134‐5p was significantly upregulated in glioma cells. The overexpression of miR‐134‐5p inhibited cell proliferation and migration of glioma cell U251 and U87. Reversely, knock‐down of miR‐134‐5p enhanced cell proliferation and migration. Both BTG‐2 and CircZNF609 are the direct targets of miR‐134‐5p, and their expression could be negatively regulated by miR‐134‐5p. CircZNF609 was significantly upregulated in U251 and U87 cells and acted as an oncogene to promote cell proliferation and cell migration of glioma cell U251 and U87. Conclusions These data proved that CircZNF609 served as a competing RNA to bind miR‐134‐5p that promoted BTG‐2 expression leading to reduced proliferation and migration of glioma cell.

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