1. Academic Validation
  2. MicroRNA-522-3p plays an oncogenic role in glioblastoma through activating Wnt/β-catenin signaling pathway via targeting SFRP2

MicroRNA-522-3p plays an oncogenic role in glioblastoma through activating Wnt/β-catenin signaling pathway via targeting SFRP2

  • Neuroreport. 2021 Jan 13;32(2):88-98. doi: 10.1097/WNR.0000000000001565.
Lingdang Zhang 1 Peng Zhang Yun Tan Qinglin Feng Rui Zhao
Affiliations

Affiliation

  • 1 Department of Neurosurgery, Chongqing Three Gorges Central Hospital, Chongqing, China.
Abstract

Background: Increasing studies have suggested that MicroRNAs (miRNAs) contribute to the occurrence and development of glioblastoma. MiR-522-3p is a novel miRNA, which has been found to modulate tumorigenesis and tumor progression. However, its pathological role and functional mechanism in glioblastoma remain elusive at present.

Method: The miR-522-3p expression in glioblastoma and adjacent normal tissues, human fetal astrocyte HA1800, and glioblastoma cell lines was detected by reverse transcription-PCR. The proliferation, migration, and invasion were detected through Cell Counting Kit-8 (CCK8) and Transwell assay, and Apoptosis was calculated through flow cytometry. The downstream target of miR-522-3p was analyzed through bioinformatics, and the correlation between miR-522-3p and secreted frizzled-related protein 2 (SFRP2) was verified through dual-luciferase reporter assay and RNA immunoprecipitation (RIP) experiment. Besides, western blot was conducted to test the level of SFRP2 and the Wnt/β-catenin pathway.

Results: MiR-522-3p was overexpressed in glioblastoma tissues compared with that in normal tissues, and the inhibition of miR-522-3p reduced cell proliferation, migration, and invasion and promoted Apoptosis in glioblastoma. Bioinformatics revealed that SFRP2 was an essential downstream target of miR-522-3p, and it inhibited the malignant biological behaviors induced by miR-522-3p and inactivated the Wnt/β-catenin pathway.

Conclusion: MiR-522-3p is an oncogene in glioblastoma by targeting SFRP2 through the Wnt/β-catenin pathway.

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