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LncRNA MIR4435‐2HG functions as a ceRNA against miR‐125a‐5p and promotes neuroglioma development by upregulating TAZ
BACKGROUND: Expression of the TAZ gene is closely related to the prognosis of glioma patients. We hoped to find long noncoding RNAs (lncRNAs) related to TAZ and a new target for glioma treatment. METHODS: TAZ‐related genes were found by dual‐luciferase reporter gene assay, and the correlation of eac...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8649364/ https://www.ncbi.nlm.nih.gov/pubmed/34714963 http://dx.doi.org/10.1002/jcla.24066 |
Sumario: | BACKGROUND: Expression of the TAZ gene is closely related to the prognosis of glioma patients. We hoped to find long noncoding RNAs (lncRNAs) related to TAZ and a new target for glioma treatment. METHODS: TAZ‐related genes were found by dual‐luciferase reporter gene assay, and the correlation of each gene was analyzed by the Pearson method. Human glioma cell lines U87 MG and U251 and glioma rats were used for cytology assays, and the related genes were transfected. We conducted immunohistochemistry, RT‐qPCR, Western blotting, CCK8 test, flow cytometry, transwell assays, clone formation analysis, and tumor weight measurements to verify the above relationship. RESULTS: We found that miR‐125a‐5p was closely related to the TAZ gene, and the lncRNA MIR4435‐2HG was closely related to miR‐125a‐5p. Both MIR4435‐2HG‐OE and TAZ increased the expression of the TAZ gene, activated the Wnt signaling pathway, inhibited apoptosis, and promoted migration and proliferation in glioma cells. Besides, it also increased the tumor volume of gliomas in a rat model subcutaneously inoculated with glioma cells. We also found miR‐125a‐5p could block the effect of MIR4435‐2HG‐OE and TAZ. CONCLUSIONS: LncRNA MIR4435‐2HG obstructs the functions of miR‐125a‐5p and promotes neuroglioma development by upregulating the TAZ gene. |
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