z-logo
open-access-imgOpen Access
Effect of miR-25 on Proliferation of Nasopharyngeal Carcinoma Cells through Wnt/β-Catenin Signaling Pathway
Author(s) -
Haixia He,
Kun Yuan,
Wei Chen
Publication year - 2021
Publication title -
biomed research international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 126
eISSN - 2314-6141
pISSN - 2314-6133
DOI - 10.1155/2021/9957161
Subject(s) - wnt signaling pathway , nasopharyngeal carcinoma , catenin , cancer research , signal transduction , carcinoma , beta catenin , biology , microbiology and biotechnology , medicine , radiation therapy
Objective To investigate the biological role and potential mechanism of miR-25 in nasopharyngeal carcinoma.Methods The expression of miR-25 in nasopharyngeal carcinoma cell lines was detected by qRT-PCR. The effect of inhibition of miR-25 expression on the proliferative activity of nasopharyngeal carcinoma cell line HONE-1 was examined by CCK-8 method. Flow cytometry was used to detect the effect of miR-25 expression inhibition on the apoptosis rate of nasopharyngeal carcinoma cell line HONE-1. The miRNA target gene prediction site TargetScan predicts the target protein action site of miR-124 and verifies whether miR-25 interacts with the target by luciferase activity assay, qPCR, and Western experiments. The miR-25 inhibitor and target egg gene expression plasmids were cotransfected into HONE-1 cells for rescue experiments to investigate whether miR-25 inhibits proliferation of nasopharyngeal carcinoma cells by target genes. At the same time, qRT-PCR was used to detect the mRNA expression levels of Wnt/ β -catenin pathway key proteins TCF4, c-Myc, and Cyclin D1 in different transfected cells.Results miR-25 expression was upregulated in nasopharyngeal carcinoma cell lines. Functional studies showed that inhibition of miR-25 expression significantly inhibited the proliferation of nasopharyngeal carcinoma cell line HONE-1 ( p < 0.05). Inhibition of miR-25 expression by flow cytometry significantly promoted apoptosis ( p < 0.05). Detection of dual luciferase activity indicated that DKK3 is a direct target site for miR-25. Western blots showed that inhibition of miR-25 significantly upregulated DKK3 mRNA and protein levels. Supplementation with DKK3 significantly attenuated the inhibitory effect of miR-25 on the proliferation of nasopharyngeal carcinoma cell line HONE-1 ( p < 0.05). qRT-PCR found that mRNA levels of TCF4, c-Myc, and Cyclin D1 were significantly upregulated in miR-25-transfected cells compared to control transfection. QRT PCR showed that the mRNA and protein levels of Tcf4, c-myc, and Cyclin D1 were significantly upregulated in miR-25 overexpression-transfected cells.Conclusion Inhibition of miR-25 expression promotes DKK3 gene expression, and inactivation of Wnt/ β -catenin signaling pathway inhibits proliferation and promotes apoptosis of nasopharyngeal carcinoma cells.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom