microRNA-106a induces the proliferation and apoptosis of glioma cells through regulating JNK/MAPK pathway

X.-H. Chen, X.-M. Ling, S. Shi

Department of Gynecology, Henan Provincial People’s Hospital, Zhengzhou, China. chenxh1895@163.com

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• Oncology

OBJECTIVE: To investigate the expression of microRNA-106a (miRNA-106a) in the brain tissue and the plasma of glioma patients, and explore the mechanism underlying the effect of miRNA-106a on the proliferation and apoptosis of glioma cells.

PATIENTS AND METHODS: Brain tissues from 42 glioma patients admitted in our institution were included in study group, whereas normal brain tissues collected from 10 patients undergoing brain tissue resection due to decompression or exposure during cerebral surgery. Quantitative fluorescent RT-PCR (QF RT-PCR) was performed to measure miRNA-106a mRNA levels in the brain tissue and peripheral blood of patients in two groups. Human M059K glioma cells were transfected with miRNA-106a mimic and inhibitor, and the proliferation and apoptosis of glioma cells were analyzed. In addition, JNK/MAPK in glioma cells was examined at mRNA and protein levels.

RESULTS: Compared with the normal population, miRNA-106a expression was significantly increased in the brain tissue of glioma patients (p<0.05). Besides, miRNA-106a expression level was significantly elevated in the plasma of peripheral blood of glioma patients (p<0.05). After the interference of miRNA-106a in M059K glioma cells, the proliferation of glioma cells was significantly reduced. However, the apoptotic regulatory factor, Bcl-2, was significantly increased, and JNK/MAPK protein level was significantly decreased. Overexpression of miRNA-106a in glioma cells resulted in significant increase in the proliferation of glioma cells and JNK/MAPK protein level, but obvious suppression in Bcl-2 protein level.

CONCLUSIONS: Elevated expression of miRNA-106a plays a crucial role in the development and progression of glioma, probably by promoting the proliferation and suppressing the apoptosis of glioma cells through the JNK/MAPK signaling pathway.

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