EHF promotes colorectal carcinoma progression by activating TGF‐β1 transcription and canonical TGF‐β signaling. Issue 7 (10th June 2020)

• Record Type: Journal Article
• Authors: Wang, Lan; Ai, Meiling; Nie, Miaoting; Zhao, Li; Deng, Guangxu; Hu, Shasha; Han, Yue; Zeng, Weiting; Wang, Yiqing; Yang, Minhui; Wang, Shuang
• Is Part Of: Cancer science. Volume 111:Issue 7(2020)
• Page Start: 2310
• Page End: 2324
• Publication Date: 2020-06-10
• Subjects: colorectal carcinoma -- EHF -- proliferation and migration -- TGF‐β signaling -- transcription factor; Cancer -- Periodicals; Neoplasms -- Periodicals; Research -- Periodicals; Electronic journals; 616.994005
• DOI: 10.1111/cas.14444
• Languages: English
• ISSNs: 1347-9032

Abstract

Abstract: ETS homologous factor (EHF) plays a critical function in epithelial cell differentiation and proliferation. However, the roles of EHF in cancer remain largely unknown. In the present study, we investigated the expression levels, precise function and mechanism of EHF in colorectal carcinoma (CRC). We observed significantly elevated EHF expression in CRC cell lines and tissues. EHF overexpression correlated positively with poor differentiation, advanced T stage, and shorter overall survival of CRC patients. Function experiments revealed that EHF overexpression promoted CRC cell proliferation, migration, and invasion in vitro and in vivo. Mechanistically, EHF could directly upregulate transforming growth factor β1 (TGF‐β1) expression at the transcription level, thereby activating canonical TGF‐β signaling. Our findings provide novel insights into the mechanisms of EHF in tumorigenesis, invasion, and metastasis of CRC, which may help to provide new therapeutic targets for CRC intervention. Abstract : 1, EHF is upregulated in colorectal carcinoma (CRC). 2, The EHF overexpressing contributes to CRC cell proliferation, invasion and metastasis in vitro and in vivo. 3, EHF is a transcript activator for promoting TGF‐β1 transcription, thereby activating the canonical TGF‐β signaling.