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

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• 作者：Shang-tong Lei^a ; ¹ ; Fei Shen^b ; ¹ ; Ji-wei Chen^b ; Jian-hua Feng^b ; Wen-song Cai^b ; Liang Shen^b ; Zhi-wen Hu^c ; Bo Xu^b ; ^{xubo_cancer@163.com}
• 关键词：MiR-639 ; Human thyroid cancer ; CDKN1A ; Cell proliferation ; Cell cycle
• 刊名：Biomedicine & Pharmacotherapy
• 出版年：2016
• 出版时间：December 2016
• 年：2016
• 卷：84
• 期：Complete
• 页码：1834-1840
• 全文大小：1849 K
• 卷排序：84

文摘

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.