MicroRNA-124-3p promotes apoptosis and autophagy of glioma cells by down-regulating CREBRF

ABSTRACT

Objective

This research was performed to dissect the influence of microRNA (miR)-124-3p on the apoptosis and autophagy of glioma cells and clarify its specific mechanism.

Methods

RT-PCR and western blot were utilized to determine miR-124-3p and CREBRF expression in U251 and T98 cells. After loss- and gain-of-function assays in U251 and T98 cells, glioma cell proliferation, autophagy, and apoptosis were measured by MTT assay, western blot, and flow cytometry, respectively. The relationship between miR-124-3p and CREBRF was examined by dual-luciferase reporter assay. The levels of AKT pathway-related proteins were detected by western blot.

Results

MiR-124-3p was lowly expressed and CREBRF was highly expressed in U251 and T98 cells. Overexpression of miR-124-3p or knockdown of CREBRF enhanced apoptosis and autophagy and diminished proliferation of glioma cells. MiR-124-3p negatively targeted CREBRF. MiR-124-3p up-regulation repressed proliferation and facilitated apoptosis and autophagy of glioma cells by diminishing CREBRF expression and blocking the AKT pathway.

Conclusion

MiR-124-3p accelerates apoptosis and autophagy of glioma cells via CREBRF.

KEYWORDS:

• Glioma cells
• microRNA-124-3p
• CREBRF
• proliferation
• autophagy
• apoptosis

Disclosure statement

No potential conflict of interest was reported by the author(s).

Availability of data and materials

The datasets used or analyzed during the current study are available from the corresponding author on reasonable request.

Author contribution

ZH conceived the ideas. GX designed the experiments. ZH and HMY performed the experiments. GX and HMY analyzed the data. ZH and HMY provided critical materials. ZH and HMY wrote the manuscript. GX supervised the study. All the authors have read and approved the final version for publication.

Correction Statement

This article has been republished with minor changes. These changes do not impact the academic content of the article.

Additional information

Funding

This research was funded by the grants from Science and Technology Planning Project of Changsha (Grant No. kq2004108).