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MiR-186 promotes the apoptosis of glioma U87 cells by down-regulating the expression of Smad6.
- Source :
- European Review for Medical & Pharmacological Sciences; 2020, Vol. 24 Issue 14, p7681-7689, 9p
- Publication Year :
- 2020
-
Abstract
- OBJECTIVE: MiRNA family gene is an evolutionarily conserved non-coding small RNA that directly participates in a variety of physiological processes and cancer development via regulating gene expression in the biological level of transcription. To research the specific mechanism by which miR-186 regulates apoptosis within gliomas. PATIENTS AND METHODS: RT-qPCR was performed to verify the transcriptional level of miR-186 within glioma tissues and glioma cells. miRanda and Dual-Luciferase assay were performed to predict and confirm that Smad6 gene is an effective target of miR-186 within glioma. The expression of Smad6 protein was tested by Western blot following cell effective transfection. Apoptosis of gliomas was analyzed by inverted fluorescence microscopy and flow cytometry. RESULTS: The mRNA level of miR-186 was suppressed within glioma tissues and glioma U87 cells. MiR-186 is associated with apoptosis in glioma. Overexpression of miR-186 promoted U87 cell apoptosis, whereas suppression of miR-186 had the opposite effect. Besides, miR-186 directly targeted Smad6 and suppress its expression in glioma. The expression of Smad6 affected the regulation of miR-186 on glioma cell apoptosis, restoration of Smad6 rescued apoptosis of glioma U87 cells induced by miR-186 mimics, whereas inhibition of Smad6 promoted apoptosis. CONCLUSIONS: As noted above, miR-186 exerts a tumor-suppressing effect by targeting Smad6. We propose that miR-186 can be used as a novel biomarker for glioma diagnosis in the future, or as a new pharmacy target in the cure of gliomas. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 11283602
- Volume :
- 24
- Issue :
- 14
- Database :
- Supplemental Index
- Journal :
- European Review for Medical & Pharmacological Sciences
- Publication Type :
- Academic Journal
- Accession number :
- 144820695