The role of miR-382-5p in glioma cell proliferation, migration and invasion

Dysregulation of a single miRNA can play an essential role in tumor development and progression. Recent studies have shown that miR-382-5p can function as an oncogene or as a tumor suppressor in different types of cancers. However, the role of miR-382-5p in glioma growth and expansion has not been characterized.

In summary, miR-382-5p inhibited proliferation, migration, invasion, and the EMT in glioma cells, possibly through targeting the oncogene YBX1.

Quantitative real time-PCR (qRT-PCR) was used to measure miR-382-5p levels in glioma tissues. The miR-382-5p mimics and inhibitors were employed to upregulate and downregulate miR-382-5p expression respectively in glioma cells. EdU assay was used to assess cell proliferation. Wound healing and Transwell assays were employed to evaluate cell migration and invasion. Western blot was used to measure the changes of epithelial-to-mesenchymal transition (EMT) markers and the potential miR-382-5p target genes.

We found that miR-382-5p levels were low in glioma tissues as determined by qRT-PCR. EdU assay showed that upregulation of miR-382-5p significantly decreased cell proliferation in both U87 and U251 cells. Wound healing rate was significantly decreased in response to miR-382-5p mimics and significantly increased in response to miR-382-5p inhibitors. Transwell migration assays further confirmed the inhibitory effects of miR-382-5p on the migration in both U251 and U87 cells. Transwell invasion assays showed that upregulation of miR-382-5p resulted in a remarkable decrease in the number of invading cells, whereas downregulation of miR-382-5p led to a significant increase in the numbers of invading U87 and U251 cells. In addition, overexpression of miR-382-5p decreased the protein levels of N-cadherin, Snail and Slug, and increased E-cadherin levels, in glioma cells. Furthermore, miR-382-5p levels negatively correlated with Y box-binding protein 1 (YBX1) in lower grade glioma tissues, and negatively regulated the expression of YBX1 in glioma cells.