miR-142-3p inhibits cancer cell proliferation by targeting CDC25C

被引:52
|
作者
Cao, Xu-Chen [1 ,2 ,3 ]
Yu, Yue [1 ,2 ,3 ]
Hou, Li-Kun [1 ,2 ,3 ]
Sun, Xiao-Hu [1 ,2 ,3 ]
Ge, Jie [1 ,2 ,3 ]
Zhang, Bin [1 ,2 ,3 ]
Wang, Xin [1 ,2 ,3 ]
机构
[1] Tianjin Med Univ Canc Inst & Hosp, Dept Breast Canc 1, Natl Clin Res Ctr Canc, Tianjin 300060, Peoples R China
[2] Key Lab Canc Prevent & Therapy, Tianjin 300060, Peoples R China
[3] Tianjin Med Univ, Key Lab Breast Canc Prevent & Therapy, Minist Educ, Tianjin 300060, Peoples R China
基金
中国国家自然科学基金;
关键词
TUMOR-SUPPRESSOR; MITOTIC EXIT; MICRORNA-142-3P; OVEREXPRESSION; PHOSPHATASES; EXPRESSION; REGULATOR; INVASION; CYCLE;
D O I
10.1111/cpr.12235
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
ObjectivesMicroRNAs (miRNAs) contribute to control of cell cycle progression and are frequently deregulated in cancer. The focus of this study was to determine effects of miR-142-3p on the cell cycle progression and cancer cell proliferation. Materials and methodsRT-qPCR was performed to determine expression of miR-142-3p in a range of cancer cell lines and in clinical cancer specimens. To further understand its role, we restored its expression in cancer cell lines by transfection with miR-142-3p mimics or inhibitors. Effects of miR-142-3p on cell cycle progression and cell proliferation were also determined. ResultsmiR-142-3p was down-regulated in both cancer cell lines and cancer specimens. Its overexpression suppressed proliferation, whereas its depletion promoted it. In addition, miR-142-3p lead to cell cycle arrest in G2/M. Moreover, CDC25C was identified as being a target of miR-142-3p, ectopic expression of which reversed suppression of cell proliferation. ConclusionsOur observations suggest that miR-142-3p functioned as a tumor suppressor by targeting CDC25C.
引用
收藏
页码:58 / 68
页数:11
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