BioScience Trends
Online ISSN : 1881-7823
Print ISSN : 1881-7815
ISSN-L : 1881-7815

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IFITM3 upregulates c-myc expression to promote hepatocellular carcinoma proliferation via the ERK1/2 signalling pathway
Jiaqi MinJunwen HuChen LuoJinfeng ZhuJiefeng ZhaoZhengming ZhuLinquan WuRongfa Yuan
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ジャーナル フリー 早期公開

論文ID: 2019.01289

この記事には本公開記事があります。
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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 downregulation of c-myc reduced the proliferation of HCC enhanced by IFITM3. Mechanistically, IFITM3 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.

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© 2019 International Research and Cooperation Association for Bio & Socio-Sciences Advancement
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