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The biological function of E26 transformation-specific (ETS) transcription factor EHF/ESE-3 in human cancers remains largely unknown, particularly gastric cancer. The aim of this study was to explore the role of EHF in tumorigenesis and its potential as a therapeutic target in gastric cancer. By using quantitative RT-PCR (qRT-PCR), immunohistochemistry (IHC) and fluorescence  in situ  hybridization (FISH) assays, we investigated the expression and copy number of  EHF  in a cohort of gastric cancers and control subjects. Specific  EHF  siRNAs was used to determine the biologic impacts and mechanisms of altered EHF expression  in vitro  and  in vivo . Dual-luciferase reporter, chromatin immunoprecipitation (ChIP) and electrophoretic mobility shift assay (EMSA) assays were performed to identify its downstream targets. Our results demonstrated that  EHF  was significantly upregulated and frequently amplified in gastric cancer tissues as compared with control subjects. Moreover,  EHF  amplification was positively correlated with its overexpression and significantly associated with poor clinical outcomes of gastric cancer patients. We also found that EHF knockdown notably inhibited gastric cancer cell proliferation, colony formation, migration, invasion and tumorigenic potential in nude mice and induced cell cycle arrest and apoptosis. Importantly, we identified EHF as a new  HER2  transcription factor and the modulator of  HER3  and  HER4  in gastric cancer. Collectively, our findings suggest that  EHF  is a novel functional oncogene in gastric cancer by regulating the human epidermal growth factor receptor (HER) family of receptor tyrosine kinases and may represent a potential prognostic marker and therapeutic target for this cancer.

cell death and disease

Increased expression of EHF via gene amplification contributes to the activation of HER family signaling and associates with poor survival in gastric cancer