ELF3 promotes epithelial–mesenchymal transition by protecting ZEB1 from miR-141-3p-mediated silencing in hepatocellular carcinoma

• DOI: 10.1038/s41419-018-0399-y
• Publication Date: 2018-03-09T10:51:15Z
• Authors: Longbo Zheng; Ming Xu; Junjie Xu; Ke Wu; Qian Fang; Yuelong Liang; Senjun Zhou; Dong Cen; Lin Ji; Weili Han; Xiujun Cai
• Keywords: Chromatin immunoprecipitation

Abstract Hepatocellular carcinoma (HCC) is one of the most common malignant cancers and currently third leading cause cancer-related deaths, worldwide. Epithelial–mesenchymal transition (EMT) plays a major role in HCC progression. In this study, we first found that expression E74-like ETS transcription factor 3 (ELF3), member E-twenty-six family factors, was increased tissues, ELF3 overexpression associated with poor prognoses for patients. Gain-of-function loss-of-function studies revealed promoted cell proliferation, migration, invasion, while these processes were inhibited when silenced. Additionally, to promote EMT, which demonstrated through decreased E-cadherin N-cadherin fibronectin expression. knockdown reversed EMT via repressing ZEB1 miR-141-3p upregulation. Chromatin immunoprecipitation assays bound promoter, suppressing Taken together, our data show repressed cells by miR-141-3p, thereby activating ZEB1. Thus, may be potential prognostic biomarker and/or therapeutic target HCC.