MiR-32 Inhibits Proliferation and Metastasis by Targeting EZH2 in Glioma

Author:

Zhang Yuan12,Wang Jiangang12,An Wenzhi3,Chen Chen4,Wang Wencheng4,Zhu Chao5,Chen Fangzhou5,Chen Huizhao5,Zheng Wei5ORCID,Gong Jie12

Affiliation:

1. Department of Neurosurgery, Qilu Hospital of Shandong University and Institute of Brain and Brain-Inspired Science, Shandong University, Jinan City, Shandong Province, People’s Republic of China

2. Shandong Key Laboratory of Brain Function Remodeling, Jinan City, Shandong Province, People’s Republic of China

3. Department of Neurosurgery, Cangzhou Central Hospital, Cangzhou City, Hebei Province, People’s Republic of China

4. Taishan Medical University, Taian City, Shandong Province, People’s Republic of China

5. Department of Neurosurgery, Affiliated Hospital of Taishan Medical University, Taian City, Shandong Province, People’s Republic of China

Abstract

Purpose: Glioma is identified as a broad category of brain and spinal cord tumors. MiR-32 is important in regulating the genesis of different cancers; however, the underlying mechanisms of miR-32 in glioma still largely unknown. This study aimed to elucidate pathobiological functions of miR-32 in glioma and verify its effect on the regulation of enhancer of zeste homolog 2. Methods: The expression of miR-32 and enhancer of zeste homolog 2 was detected by quantitative real-time polymerase chain reaction and Western blot in glioma tissues and cells. Cell Counting Kit-8 (CCK-8) assay was used to examine the effects of miR-32 on human glioma cells proliferation. Transwell assay was used to examine cell metastasis, respectively. Two bioinformatics analysis software and luciferase reporter assay were chosen to confirm targeting association between miR-32 and enhancer of zeste homolog 2. Results: MiR-32 was downregulated in glioma tissues and cells. Furthermore, enhancer of zeste homolog 2 expression was upregulated and negatively correlated with miR-32 in clinical tissues. Ectopic expression of miR-32 inhibited glioma cell proliferation, migration, and invasion. Enhancer of zeste homolog 2 was identified as direct target gene of miR-32 in glioma. Overexpression of enhancer of zeste homolog 2 ablated the inhibitory effects of miR-32. Conclusion: In summary, our finding suggests that miR-32 acts an important role in inhibiting glioma cell proliferation and metastasis and suppresses the expression of ABCC4 by directly targeting its 3′-untranslated region. The miR-32/enhancer of zeste homolog 2 axis may provide new insights to the treatment for glioma.

Publisher

SAGE Publications

Subject

Cancer Research,Oncology

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