| Literature DB >> 27645894 |
Xuhui Gao1, Xuelian Wang2, Kaican Cai3, Wujun Wang3, Qun Ju3, Xiyao Yang3, Haofei Wang3, Hua Wu4.
Abstract
In this study, we investigated the expression patterns and functional roles of microRNA 127 (miR-127) and its target gene Formin-Like 3 (FMNL3) in human esophageal squamous cell carcinoma (ESCC). Quantitative RT-PCR (qRT-PCR) was used to compare miR-127 expression between ESCC cell lines and normal esophageal epithelium cell line, as well as paired ESCC tumors and adjacent normal esophageal tissues in 33 patients. We found miR-127 was aberrantly downregulated in both ESCC cell lines and human ESCC tumors. In ESCC cell lines TE-1 and ECA109 cells, lentiviral-induced miR-127 upregulation markedly inhibited cancer proliferation and migration in vitro, and tumorigenicity in vivo. Through dual-luciferase assay and qRT-PCR, FMNL3 was confirmed to be the downstream target gene of miR-127 in ESCC. Finally, FMNL3 was downregulated by siRNA in TE-1 and ECA109 cells. And we discovered that SiRNA-induced FMNL3 downregulation had tumor suppressive effect in ESCC, inhibiting cancer proliferation, migration in vitro, and tumorigenicity in vivo. These results suggest that miR-127 is downregulated and acting as tumor suppressor in ESCC. Inversely, FMNL3, the target gene of miR-127, is upregulated and acting as an oncogene in ESCC.Entities:
Keywords: Cancer in vitro growth; Cancer in vivo growth, FMNL3; Esophageal squamous cell carcinoma; MiR-127
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Year: 2016 PMID: 27645894 DOI: 10.1016/j.ejphar.2016.09.025
Source DB: PubMed Journal: Eur J Pharmacol ISSN: 0014-2999 Impact factor: 4.432