Upregulated miR‐106a plays an oncogenic role in pancreatic cancer. Issue 5 (18th January 2014)

• Record Type: Journal Article
• Authors: Li, Pei; Xu, Qinhong; Zhang, Dong; Li, Xuqi; Han, Liang; Lei, Jianjun; Duan, Wanxing; Ma, Qingyong; Wu, Zheng; Wang, Zheng
• Is Part Of: FEBS letters. Volume 588:Issue 5(2014)
• Page Start: 705
• Page End: 712
• Publication Date: 2014-01-18
• Subjects: Pancreatic cancer -- miRNA -- miR-106a -- Cell invasion -- Tissue inhibitors of metalloproteinase 2; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1016/j.febslet.2014.01.007
• Languages: English
• ISSNs: 0014-5793

Abstract

Abstract : Carcinogenesis is a complex process during which cells undergo genetic and epigenetic alterations. MicroRNAs control gene expression by negatively regulating protein‐coding mRNAs. Several reports demonstrated that miR‐106a is up‐regulated in gastric and colorectal cancers and promotes tumor progression. In contrast, in glioma miR‐106a plays the role of a tumor suppressor gene rather than an oncogene. Here we demonstrate that a high level of miR‐106a expression is present in pancreatic cancer. Furthermore, our investigation shows that miR‐106a has an oncogenic role in pancreatic tumorigenesis by promoting cancer cell proliferation, epithelial–mesenchymal transition and invasion by targeting tissue inhibitors of metalloproteinase 2 ( TIMP‐2 ). MiR‐106a could be a critical therapeutic target in pancreatic cancer. Abstract : miR‐106a is overexpressed and plays an oncogenic role in pancreatic cancer. miR‐106a overexpression is associated with epithelial–mesenchymal transition. miR‐106a targets TIMP‐2 and further promotes pancreatic cancer cell invasion. Blocking TIMP‐2 gene mimics the function of miR‐106a.