IFITM3 upregulates c-myc expression to promote hepatocellular carcinoma proliferation via the ERK1/2 signalling pathway

被引:16
作者
Min, Jiaqi [1 ,2 ]
Hu, Junwen [1 ,3 ]
Luo, Chen [1 ]
Zhu, Jinfeng [1 ]
Zhao, Jiefeng [1 ]
Zhu, Zhengming [1 ]
Wu, Linquan [1 ]
Yuan, Rongfa [1 ]
机构
[1] Nanchang Univ, Affiliated Hosp 2, Dept Gen Surg, 1 Minde Rd, Nanchang 330006, Jiangxi, Peoples R China
[2] Aviat Gen Hosp Beijing, Dept Gen Surg, Beijing, Peoples R China
[3] Guangxi Med Univ, Canc Hosp, Dept Hepatobiliary Surg, Nanning, Peoples R China
基金
中国国家自然科学基金;
关键词
IFITM3; c-myc; hepatocellular carcinoma; ERK1/2 signalling pathway; proliferation; INDUCED TRANSMEMBRANE PROTEIN-3; BETA-CATENIN; CELL-GROWTH; INVASION; METASTASIS; RECEPTOR;
D O I
10.5582/bst.2019.01289
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Interferon-induced transmembrane protein 3 (IFITM3) is associated with cancer development. Proto-oncogene c-myc can promote tumor proliferation. However, collections of IFITM3 and c-myc in hepatocellular carcinoma (HCC) and the potential role and mechanisms of IFITM3 in c-myc-mediated tumor proliferation remain unclear. In this study, we investigated a positive correlation between the expression of IFITM3 and c-myc in HCC. The down-regulation of IFITM3 significantly reduced c-myc expression and inhibited the proliferation of HCC in vitro and in vivo. In addition, upregulated c-myc expression restored the decrease in cell proliferation caused by the downregulation of IFITM3, while down regulation of c-myc reduced the proliferation of HCC enhanced by IFITM3. Mechanisticall, IF ITM3 regulates c-myc expression via the ERK1/2 signalling pathway. In conclusion, a novel path of IFITM3-ERK1/2-c-myc regulatory circuitry was identified. and its dysfunction may lead to HCC tumorigenesis.
引用
收藏
页码:523 / 529
页数:7
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