MicroRNA-7 functions as a tumor-suppressor gene by regulating ILF2 in pancreatic carcinoma

被引:62
作者
Bi, Yiliang [1 ]
Shen, Wei [1 ]
Min, Min [1 ]
Liu, Yan [1 ]
机构
[1] Acad Mil Med Sci, Dept Gastroenterol, PLA, Hosp 307, 8 East St, Beijing 100071, Peoples R China
关键词
pancreatic carcinoma; interleukin enhancer binding factor 2; microRNA-7; curcumin; EPITHELIAL-MESENCHYMAL TRANSITION; CANCER-CELL-MIGRATION; LIVER-CANCER; E-CADHERIN; EXPRESSION; INVASION; NF45; ADENOCARCINOMA; RNA; PROLIFERATION;
D O I
10.3892/ijmm.2017.2894
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
100103 [病原生物学]; 100218 [急诊医学];
摘要
Interleukin enhancer binding factor 2 (ILF2) has been found to be markedly upregulated in pancreatic carcinoma and is involved in the pathogenesis of pancreatic carcinoma. Thus, ILF2 may be a potential target for therapy. Yet, the regulatory mechanisms of ILF2 in pancreatic carcinoma remain largely elusive. In the present study, we demonstrated that ILF2 functioned as an oncogene and regulated epithelial-mesenchymal transition (EMT)-associated genes in pancreatic carcinoma PANC-1 cells. MicroRNA-7 (miR-7) suppressed ILF2 mRNA expression and the protein level in PANC-1 cells. Contrary to ILF2, miRNA-7 functioned as a tumor-suppressor gene and negatively regulated EMT-associated genes in the PANC-1 cells. Curcumin, a polyphenol natural product isolated from the rhizome of the plant Curcuma longa, has emerged as a promising anticancer therapeutic agent. We found that treatment with curcumin increased miR-7 expression and suppressed ILF2 protein in the PANC-1 cells. Thus, we identified ILF2 as a new downstream target gene of curcumin. The results revealed that ILF2 is regulated by miR-7 and suggest that downregulation of miR-7 may be an important factor for the ILF2 overexpression in pancreatic carcinoma.
引用
收藏
页码:900 / 906
页数:7
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