MiR-639 promoted cell proliferation and cell cycle in human thyroid cancer by suppressing CDKN1A expression

被引:30
作者
Lei, Shang-tong [1 ]
Shen, Fei [2 ]
Chen, Ji-wei [2 ]
Feng, Jian-hua [2 ]
Cai, Wen-song [2 ]
Shen, Liang [2 ]
Hu, Zhi-wen [3 ]
Xu, Bo [2 ]
机构
[1] Southern Med Univ, Nanfang Hosp, Dept Gen Surg, Guangzhou 510515, Guangdong, Peoples R China
[2] Guangzhou Med Univ, Guangzhou Peoples Hosp 1, Dept Thyroid Surg, 1 Panfu Rd, Guangzhou 510180, Guangdong, Peoples R China
[3] Guangzhou Med Univ, Guangzhou Peoples Hosp 1, Dept Med Ultrasound, Guangzhou 510180, Guangdong, Peoples R China
关键词
MiR-639; Human thyroid cancer; CDKN1A; Cell proliferation; Cell cycle; CARCINOMA; GROWTH; INVASION; METASTASIS;
D O I
10.1016/j.biopha.2016.10.087
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Accumulating evidence has indicated that aberrantly expressed microRNAs (miRs) are extensively involved in cancer development and progression. MiR-639 has been reported to act as tumor promoter in various types of cancer. However, the biological function and underlying molecular mechanism of miR-639 in thyroid carcinoma (TC) have not been intensively investigated. Herein the present study aimed to investigate the functional role of miR-639 in TC. We found that miR-639 expression was upregulated in TC cells and clinical tissues. Overexpression of miR-639 promoted TC cell proliferation and cell cycle, with increased expression of CyclinE and c-myc, whereas miR-639-in reverses the function. Using prediction software and luciferase reporter assay, we found that CDKN1A was a target of miR-639. CDKN1A small interfering RNA (siRNA) abrogated the role of miR-639-in on cell proliferation of TC. In summary, our data demonstrated that miR-639 upregulation was associated with development of TC, miR-639 promoted cell proliferation and cell cycle by targeting CDKN1A in TC. (C) 2016 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:1834 / 1840
页数:7
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