miR-182-5p Promotes Growth in Oral Squamous Cell Carcinoma by Inhibiting CAMK2N1

被引:46
|
作者
Li, Nan [1 ]
Nan, Chuan-Chuan [2 ]
Zhong, Xue-Yun [3 ]
Weng, Jun-Quan [1 ]
Fan, Hai-Dong [1 ]
Sun, Hai-Peng [1 ]
Tang, Su [1 ]
Shi, Lei [1 ]
Huang, Sheng-Xing [1 ]
机构
[1] Jinan Univ, Clin Med Sch 2, Shenzhen Peoples Hosp, Dept Stomatol Ctr, Shenzhen 518020, Guangdong, Peoples R China
[2] Jinan Univ, Clin Med Sch 2, Shenzhen Peoples Hosp, Dept Intens Care Unit, Shenzhen, Peoples R China
[3] Jinan Univ, Basic Med Sch, Guangzhou, Guangdong, Peoples R China
关键词
Oral squamous cell carcinoma; MicroRNAs; CAMK2N1; Proliferation; PROSTATE-CANCER; INVASION; EXPRESSION; APOPTOSIS; MIGRATION; RECEPTOR;
D O I
10.1159/000493411
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Background/Aims: Emerging evidence suggests that the propagation of oral squamous cell carcinoma (OSCC) is influenced by the abnormal expression of microRNAs (miRNAs). This study aimed to characterize the involvement of mi R-182-5p in OSCC by targeting the calcium/calmodulin-dependent protein kinase II inhibitor CAMK2N1. Methods: mi R-182-5p expression was quantified in OSCC tissues and cell lines with reverse transcription polymerase chain reaction (RT-PCR). Cell colony formation, Cell Counting Kit-8 (CCK-8), Ki-67, and nude mouse xenograft assays were used to characterize the role of miR-182-5p in the proliferation of OSCC. A miR-182-5p target gene was identified with western blotting, RT-PCR, and luciferase activity assays. OSCC patient survival based on CAMK2N1 expression was also analyzed. Results: miR-182-5p was up-regulated in in vitro cell lines and in vivo clinical OSCC samples. CCK-8, colony formation, and Ki-67 assays revealed that miR-182-5p promoted the growth and proliferation of OSCC cells. miR-182-5p directly targeted CAMK2N1, as evidenced by luciferase assays and target prediction algorithms. CAMK2N1 operated as a tumor suppressor gene in patients with OSCC. Down-regulating miR-182-5p expression in the CAL-27 cell line restored CAMK2N1-mediated OSCC cell proliferation. miR-182-5p expression inhibited the activation of AKT, ERK1/2, and NF-KB. Mice injected with CAL-27 cells transfected with mi R182-5p-inhibitor demonstrated a significant increase in tumor size and weight and increased CAMK2N1 mRNA and protein expression compared with the miR-negative control group. Conclusion: The miR-182-5p-CAMK2N1 pathway can be potentially targeted to regulate the proliferation of OSCC cells. (C) 2018 The Author(s) Published by S. Karger AG, Basel
引用
收藏
页码:1329 / 1341
页数:13
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