MicroRNA-32 (miR-32) regulates phosphatase and tensin homologue (PTEN) expression and promotes growth, migration, and invasion in colorectal carcinoma cells

Molecular Cancer

Research

Xiao Feng¹  Weiyun Wu¹  Hao Wang¹  Shicai Ye¹  Guoli Wei¹  Wenkai Tan¹  Pengchun Yang¹  Yu Zhou¹  Jingfang Yang¹ 

[1] Department of Gastroenterology, The affiliated Hospital of Guangdong Medical College, South Peoples Avenue No. 57, Xiashan District, Zhanjiang, Guangdong, China;

关键词: microRNA;    Colorectal carcinoma;    PTEN;    Invasion;   

DOI  :  10.1186/1476-4598-12-30

 received in 2012-12-08, accepted in 2013-04-17,  发布年份 2013

来源: Springer

【 摘 要 】

BackgroundColorectal carcinoma (CRC) is one of the leading causes of cancer-related mortality worldwide. MicroRNAs (miRNAs, miRs) play important roles in carcinogenesis. MiR-32 has been shown to be upregulated in CRC. In this study, we identified the potential effects of miR-32 on some important biological properties of CRC cells, and clarified the regulation of PTEN by miR-32.MethodsThe effect of miR-32 on PTEN expression was assessed in CRC cell lines with miR-32 mimics/inhibitor to increase/decrease miR-32 expression. Furthermore, the roles of miR-32 in regulating CRC cells biological properties were analyzed with miR-32 mimics/inhibitor-transfected cells. The 3′-untranslated region (3′-UTR) of PTEN combined with miR-32 was verified by dual-luciferase reporter assay.ResultsGain-of-function and loss-of-function studies showed that overexpression of miR-32 promoted SW480 cell proliferation, migration, and invasion, reduced apoptosis, and resulted in downregulation of PTEN at a posttranscriptional level. However, miR-32 knock-down inhibited these processes in HCT-116 cells and enhanced the expression of PTEN protein. In addition, we further identified PTEN as the functional downstream target of miR-32 by directly targeting the 3′-UTR of PTEN.ConclusionsOur results demonstrated that miR-32 was involved in tumorigenesis of CRC at least in part by suppression of PTEN.

【 授权许可】

Unknown   
© Wu et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.