IFITM3 upregulates c-myc expression to promote hepatocellular carcinoma proliferation via the ERK1/2 signalling pathway
IFITM3 upregulates c-myc expression to promote hepatocellular carcinoma proliferation via the ERK1/2 signalling pathway
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IFITM3 通过 ERK1/2 信号通路上调 c-myc 表达，促进肝细胞癌增殖。
DOI：
10.5582/bst.2019.01289
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发表时间：
2019-12-01
影响因子：
5.5
通讯作者：
Yuan, Rongfa
中科院分区：
文献类型：
--
作者：
Min, Jiaqi;Hu, Junwen;Yuan, Rongfa
干扰素诱导的跨膜蛋白3（IFITM 3）与癌症的发展有关。原癌基因c-myc可促进肿瘤增殖。然而，IFITM 3和c-myc在肝细胞癌（HCC）中的聚集以及IFITM 3在c-myc介导的肿瘤增殖中的潜在作用和机制仍不清楚。在这项研究中，我们研究了肝癌中IFITM 3和c-myc的表达之间的正相关性。IFITM 3的下调可显著降低c-myc的表达，抑制肝癌细胞的增殖。此外，上调c-myc表达恢复了由IFITM 3下调引起的细胞增殖的下降，而下调c-myc降低了由IFITM 3增强的HCC增殖。IFITM 3通过ERK 1/2信号通路调节c-myc的表达。总之，IFITM 3-ERK 1/2-c-myc调控通路的新途径被确定，其功能障碍可能导致HCC肿瘤发生。
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.