Oxytocin inhibits head and neck squamous cell carcinoma cell migration by early growth response-1 upregulation

被引:13
作者
Kim, Jinkyung [1 ,2 ]
Kang, Sung-Min [1 ,2 ]
Lee, Heon-Jin [1 ,2 ]
Choi, So-Young [3 ]
Hong, Su-Hyung [1 ,2 ]
机构
[1] Kyungpook Natl Univ, Sch Dent, Dept Oral Microbiol, Daegu, South Korea
[2] Kyungpook Natl Univ, Sch Dent, Dept Immunol, Daegu, South Korea
[3] Kyungpook Natl Univ, Sch Dent, Dept Oral & Maxillofacial Surg, Daegu, South Korea
基金
新加坡国家研究基金会;
关键词
cell migration; early growth response-1; head and neck squamous cell carcinoma; three-dimensional cell culture; EPITHELIAL-MESENCHYMAL TRANSITIONS; EGR-1 TRANSCRIPTION FACTOR; CANCER CELLS; NUCLEAR TRANSLOCATION; PTEN EXPRESSION; STEM-CELLS; IN-VITRO; RECEPTOR; PROTEIN; MOUSE;
D O I
10.1097/CAD.0000000000000501
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The effect of oxytocin (OXT) on cancer invasion is controversial. Few studies have examined the effect of early growth response-1 (EGR1) on the invasion of head and neck squamous cell carcinoma (HNSCC). Here, we evaluated how EGR1 affects HNSCC cell migration through the molecular mechanism of OXT in exerting anti-invasion activity. Matrigel invasion and wound-healing assays were used to measure the in-vitro cell migration. The molecular mechanism of OXT was assessed by knockdown or overexpression of EGR1 in HNSCC cells. Three-dimensional (3-D) spheroids formation, followed by the image analysis for quantification was performed. OXT at 500 nmol/l increased mRNA and protein expression of E-cadherin without cytotoxicity. OXT upregulated mRNA and protein expression of EGR1 in 6 h. p53, phosphatase and tensin, and p21 expression was increased in an EGR1-dependent manner with OXT treatment. In addition, OXT significantly downregulated 3-D spheroids' formation according to spheroids' number and size. Our data showed that OXT downregulated HNSCC cell migration by EGR1 upregulation. OXT inhibited spheroids' formation of HNSCC cells under 3-D culture conditions. Copyright (C) 2017 Wolters Kluwer Health, Inc. All rights reserved.
引用
收藏
页码:613 / 622
页数:10
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