• Weiyun Wu, Jingfang Yang, Xiao Feng, Hao Wang, Shicai Ye, Pengchun Yang, Wenkai Tan, Guoli Wei, and Yu Zhou.
• Department of Gastroenterology, The affiliated Hospital of Guangdong Medical College, Zhanjiang, Guangdong, China.
• Mol Cancer. 2013 Apr 23; 12: 30.

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.

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