RETRACTED ARTICLE: LncRNA RP11-84E24.3 drives tumorigenesis and epithelial-to-mesenchymal transition of glioma cells by promoting TFAP2C-mediated activation of SNAI1
| Autor: | Jiang Zhang, Fuling Zhou, Dali Wang, Lisha Chang, Yunhe Zhang, Rui-Ying Chen, Jingyue Wang |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Cancer Research
Gene knockdown Chemistry Tumor initiation medicine.disease medicine.disease_cause eye diseases 03 medical and health sciences 0302 clinical medicine Neurology Oncology 030220 oncology & carcinogenesis Glioma SNAI1 Cancer research medicine Gene silencing Neurology (clinical) Epithelial–mesenchymal transition Epigenetics Carcinogenesis 030217 neurology & neurosurgery |
| Zdroj: | Journal of Neuro-Oncology. 151:157-171 |
| ISSN: | 1573-7373 0167-594X |
| DOI: | 10.1007/s11060-020-03624-3 |
| Popis: | Long noncoding RNAs (LncRNAs) are essential epigenetic regulators with critical roles in tumor initiation and malignant progression; however, the mechanism by which aberrantly expressed lncRNA RP11-84E24.3 regulates the pathogenesis of glioma is not fully understood. Here, we investigate the function of lncRNA RP11-84E24.3 in glioma onset and progression as well as identify a molecular pathway regulated by this lncRNA. Differentially expressed lncRNAs related to glioma were identified. The aberrant expression of lncRNA RP11-84E24.3 was verified in samples from patients with glioma as well as glioma cell lines. The role of lncRNA RP11-8424.3 in proliferation, apoptosis, migration, and invasion was assessed using gain- and loss-of function approaches, EdU incorporation, flow cytometry, wound healing and Transwell invasion assays. Western blot analysis was utilized to examine the expression of proteins associated with epithelial-to-mesenchymal transition (EMT). The interaction between lncRNA RP11-84E24.3, TFAP2C and SNAI1 was confirmed using RNA pull-down, ChIP and luciferase reporter assays. LncRNA RP11-84E24.3 was up-regulated in both glioma tissues and cell lines. LncRNA RP11-84E24.3 overexpression enhanced the proliferation, migration and invasion of glioma cells while reducing apoptosis. This was associated with a decrease in E-cadherin expression and an increase in N-cadherin and Vimentin expression. LncRNA RP11-84E24.3 directly targeted TFAP2C protein, resulting in increased SNAI1 expression. Knockdown of TFAP2C or SNAI1 reversed the effects of lncRNA RP11-84E24.3 overexpression, while silencing lncRNA RP11-84E24.3 inhibited tumor formation of glioma cells in vivo. LncRNA RP11-84E24.3 increased SNAI1 expression by forming a complex with TFAP2C protein, promoting EMT in glioma cells and tumor formation. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink