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MicroRNA-296-5p inhibits cell metastasis and invasion in nasopharyngeal carcinoma by reversing transforming growth factor-β-induced epithelial–mesenchymal transition

Authors :
Xudong Tang
Jing Ren
Mei-Hui Chen
Hai-qing Luo
Wen-Jia Hu
Qiu-Qin Dai
Xiangyong Li
Keyuan Zhou
Chen Chen
Source :
Cellular & Molecular Biology Letters, Vol 25, Iss 1, Pp 1-13 (2020), Cellular & Molecular Biology Letters
Publication Year :
2020
Publisher :
BMC, 2020.

Abstract

Aim To explore the effect of miR-296-5p on the metastasis of nasopharyngeal carcinoma (NPC) cells and investigate the underlying mechanism. Methods The expressions of miR-296-5p in NPC tissues and cells were determined using GSE32920 database analysis and real-time PCR and miRNA microarray assays. An miR-296-5p mimic and inhibitor were transfected into NPC cells. Then, immunofluorescence imaging, scratch wound-healing, transwell migration and invasion assays were used to observe the effects of miR-296-5p on cell metastasis and invasion. Real-time PCR and western blotting were carried out to detect the expressions of genes and proteins related to epithelial–mesenchymal transition (EMT). A dual luciferase reporter assay was used to identify whether TGF-β is the target gene of miR-296-5p. Finally, TGF-β expression plasmids were transfected into NPC cells to verify the role of TGF-β in the miR-296-5p-mediated inhibition of nasopharyngeal carcinoma cell metastasis. Results Our results show that miR-296-5p inhibits the migratory and invasive capacities of NPC cells by targeting TGF-β, which suppresses EMT. Importantly, the miR-296-5p level was significantly lower in human NPC tissues than in adjacent normal tissues. It also negatively correlated with TGF-β and was significantly associated with the lymph node metastasis of patients with NPC. Conclusions Our findings show that miR-296-5p represses the EMT-related metastasis of NPC by targeting TGF-β. This provides new insight into the role of miR-296-5p in regulating NPC metastasis and invasiveness.

Details

Language :
English
ISSN :
16891392 and 14258153
Volume :
25
Issue :
1
Database :
OpenAIRE
Journal :
Cellular & Molecular Biology Letters
Accession number :
edsair.doi.dedup.....1efcf2e52f1c104092bcb18d3ce183f6
Full Text :
https://doi.org/10.1186/s11658-020-00240-x