NEUROLOGY / BASIC RESEARCH
MiR-330-3p functions as a tumor suppressor that regulates glioma cell proliferation and migration by targeting CELF1
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Tao Li 1
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1
Department of Neurosurgery, Affiliated Hospital of Hebei University of Engineering, Handan, Hebei, China
2
Department of Cardiology, Affiliated Hospital of Hebei University of Engineering, Handan, Hebei, China
Submission date: 2017-09-05
Final revision date: 2017-11-25
Acceptance date: 2017-12-24
Online publication date: 2020-05-08
Publication date: 2020-08-06
 
Arch Med Sci 2020;16(5):1166–1175
 
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ABSTRACT
Introduction:
Glioma is a common type of neoplasm that occurs in the central nervous system. miRNAs have been demonstrated to act as critical regulators of carcinogenesis and tumor progression in multiple cancers, but the molecular mechanism of miR-330-3p in glioma remained unclear. The purpose of the study was to explore the role of miR-330-3p in glioma cell reproduction and migration.

Material and methods:
The expression levels of miR-330-3p and CELF1 in 27 glioma tissue specimens and human glioma cell lines were examined by qRT-PCR and western blot. The TargetScan database was used to predict the relationship between miR-330-3p and CELF1. Then the target relationship was verified using dual-luciferase reporter assay. The effects of miR-330-3p/CELF1 on glioma cell proliferation were evaluated by MTT and colony formation assay. Wound healing assay was employed to measure the migration ability of glioma cells.

Results:
MiR-330-3p was found lowly expressed in glioma tissues and cells compared with adjacent tissues and normal astrocytes, while CELF1 expression was relatively high in the glioma tissues and cells. Dual-luciferase reporter assay confirmed that miR-330-3p could directly target CELF1. Furthermore, miR-330-3p could down-regulate the expression of CELF1, therefore suppressing glioma cell reproduction and migration.

Conclusions:
MiR-330-3p inhibited the propagation and migration of glioma cells by repressing CELF1 expression.

eISSN:1896-9151
ISSN:1734-1922