| Literature DB >> 34048322 |
Yang Nan1,2,3, Liyun Guo4, Yalin Lu1, Gaochao Guo5, Rujun Hong1, Liwen Zhao2, Le Wang1,2, Bingcheng Ren1,2, Kai Yu1, Yue Zhong1,2,3, Qiang Huang1,2,3.
Abstract
The metastasis of tumor cells is a challenge for the clinical treatment of glioma. Epithelial-mesenchymal transition (EMT) contributes to glioma cell invasiveness. Our previous study confirmed that the expression of miRNA-451, which inhibits the PI3K/Akt signaling pathway by directly targeting CAB39 and plays a repressive role in glioma, is downregulated in glioma. However, the specific mechanism of miRNA-451 regulation in glioma is unclear. In this study, we investigated whether miRNA-451 blocks the processes of EMT and metastasis in glioma cells in vivo and in vitro. By targeting CAB39, miRNA-451 likely triggers the PI3K/Akt/Snail signaling pathway to reduce glioma proliferation, invasion, migration and EMT. We used Western blotting experiments to demonstrate that overexpression of miRNA-451 significantly reduced p-AKT(Ser473), N-cadherin, Vimentin, Twist, Snail and Cyclin D1 expression and increased E-cadherin expression. We demonstrated that overexpression of miR-451 suppressed glioma cell proliferation, invasion, migration and EMT by MTT and colony formation assays, Transwell assays, wound healing assays and animal experiments. Taken together, these results suggest that miRNA-451 can reduce EMT and metastasis in glioma cells through the suppression of the PI3K/Akt/Snail signaling pathway by targeting CAB39 in vitro and in vivo. miR-451 may be a new target for glioma treatment.Entities:
Keywords: CAB39; EMT; Glioma; Pi3k/Akt/Snail signaling pathway; miRNA-451
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Year: 2021 PMID: 34048322 PMCID: PMC8331032 DOI: 10.1080/15384101.2021.1933303
Source DB: PubMed Journal: Cell Cycle ISSN: 1551-4005 Impact factor: 5.173