Kaiso (ZBTB33) Downregulation by Mirna-181a Inhibits Cell Proliferation, Invasion, and the Epithelial–Mesenchymal Transition in Glioma Cells

• Main Authors: Ligang Wang, Jichao Ma, Xiaoxiong Wang, Fei Peng, Xin Chen, Bingjie Zheng, Chunlei Wang, Zhibo Dai, Jing Ai, Shiguang Zhao
• Format: Article
• Language: English
• Published: Cell Physiol Biochem Press GmbH & Co KG 2018-07-01
• Series: Cellular Physiology and Biochemistry
• Subjects: Glioma; MiRNA-181a; Kaiso; Proliferation; Invasion; EMT
• Online Access: https://www.karger.com/Article/FullText/491963
• ISSN: 1015-8987; 1421-9778

Background/Aims: Kaiso (ZBTB33) expression is closely associated with the progression of many cancers and microRNA (miRNA) processing. MiR-181a plays critical roles in multiple cancers; however, its precise mechanisms in glioma have not been well clarified. The goal of this study was to evaluate the interaction between Kaiso and miR-181a in glioma. Methods: Quantitative real-time PCR (qRT-PCR) was performed to detect the levels of Kaiso and miR-181a in glioma tissues and cell lines. Cell proliferation, invasion, and the epithelial–mesenchymal transition (EMT) were evaluated to analyze the biological functions of miR-181a and Kaiso in glioma cells. The mRNA and protein levels of Kaiso were measured by qRT-PCR and western blotting, respectively. Meanwhile, luciferase assays were performed to validate Kaiso as a miR-181a target in glioma cells. Results: We found that the level of miR-181a was the lowest among miR-181a–d in glioma tissues and cell lines, and the low level of miR-181a was closely associated with the increased expression of Kaiso in glioma tissues. Moreover, transfection of miR-181a significantly inhibited the proliferation, invasion, and EMT of glioma cells, whereas knockdown of miR-181a had the opposite effect. Bioinformatics analysis predicted that Kaiso was a potential target gene of miR-181a, and the luciferase reporter assay demonstrated that miR-181a could directly target Kaiso. In addition, Kaiso silencing had similar effects as miR-181a overexpression in glioma cells, whereas overexpression of Kaiso in glioma cells partially reversed the inhibitory effects of the miR-181a mimic. Conclusionss: miR-181a inhibited the proliferation, invasion, and EMT of glioma cells by directly targeting and downregulating Kaiso expression.