Research Paper Volume 11, Issue 3 pp 921—932
MicroRNA-141 suppresses growth and metastatic potential of head and neck squamous cell carcinoma
- 1 Department of Oral and Maxillofacial Surgery, Shengjing Hospital of China Medical University, Shenyang, P.R.China
- 2 Department of Clinical Laboratory, Shengjing Hospital of China Medical University, Shenyang, P.R.China
received: September 12, 2018 ; accepted: January 21, 2019 ; published: February 8, 2019 ;https://doi.org/10.18632/aging.101791
How to Cite
Copyright: Zhao et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
MicroRNAs (miRNAs) serve as regulatory factors in both healthy tissue and various cancers. Here, we used an miRNA microarray to screen for miRNAs differentially expressed between HNSCC and adjacent epithelial tissue. Among these, levels of miR-141 were significantly reduced in HNSCC tissues. Expression levels of epidermal growth factor receptor (EGFR) were enhanced in tissues with low miR-141 expression but were reduced by miR-141 overexpression, and there was a significant negative correlation between EGFR and miR-141 levels in HNSCC tissues (P < 0.01). Luciferase assays confirmed that miR-141 targeted EGFR mRNA. In vitro, miR-141 inhibited the proliferation and migration of Cal-27 and FaDu HNSCC cells with corresponding decreases in CDK4 and MMP2. miR-141 also enhanced the incidence of apoptosis among the cells with a corresponding decrease in bcl-2. In BALB/c mice injected with FaDu HNSCC cells, miR-141 mitigated hepatic metastasis and inhibited expression of EGFR, CDK4, bcl-2 and MMP2. These results suggest that miR-141 functions as a tumor suppressor in HNSCC and that it suppresses tumor growth and metastasis by suppressing EGFR signaling. MiR-141 thus appears to be a potentially useful therapeutic target in the treatment of HNSCC.