MiR-331-3p functions as an oncogene by targeting ST7L in pancreatic cancer. (30th May 2018)

• Record Type: Journal Article
• Authors: Chen, Xiaoli; Luo, Hesheng; Li, Xiaoyi; Tian, Xia; Peng, Bo; Liu, Shuiyi; Zhan, Ting; Wan, Yiyuan; Chen, Weiqun; Li, Yong; Lu, Zhongxin; Huang, Xiaodong
• Is Part Of: Carcinogenesis. Volume 39:Number 8(2018)
• Page Start: 1006
• Page End: 1015
• Publication Date: 2018-05-30
• Subjects: Carcinogenesis -- Periodicals; Cancer -- Genetic aspects -- Periodicals; Cancer -- Prevention -- Periodicals; Cancer -- Periodicals; 616.994071
• DOI: 10.1093/carcin/bgy074
• Languages: English
• ISSNs: 0143-3334

Abstract

Abstract : miR-331-3p was a tumor-promoting miRNA in PC cells and a promising biomarker for PC. Downregulation of miR-331-3p inhibited PC cell proliferation and EMT-mediated metastasis in vitro and in vivo by promoting ST7L expression. We describe a specific mechanism that explains the effects of miR-331-3p in PC. Abstract: Pancreatic cancer (PC) is a highly invasive tumor with early metastasis and poor prognosis, yet the mechanisms for tumor progression have not been fully elucidated. Emerging evidence indicates that microRNA-331-3p (miR-331-3p) plays an important role in the progression of diverse human cancers. Here, we found that miR-331-3p was significantly upregulated in tumor specimens of PC patients and PC cell lines. Functional studies showed that downregulation of miR-331-3p inhibited PC cell proliferation and epithelial–mesenchymal transition (EMT)-mediated metastasis in vitro . Furthermore, suppression of tumorigenicity 7 like ( ST7L ) was identified as a novel target gene of miR-331-3p. Tumor promotion effects of miR-331-3p were partially reversed by ST7L re-expression. In addition, miR-331-3p antagomir suppressed PC tumor growth and metastasis via upregulation of ST7L in xenograft mice. In summary, these results demonstrate that miR-331-3p is a tumor-promoting microRNA (miRNA) in PC cells and a promising biomarker for PC.