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

来源：

CELL PROLIFERATION | 2016年 / 49卷 / 01期

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

页码：58 / 68

页数：11

共 29 条

[1] MicroRNAs: Target Recognition and Regulatory Functions [J].