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首页> 外文期刊>FEBS Open Bio >IFITM3 promotes hepatocellular carcinoma invasion and metastasis by regulating MMP9 through p38/MAPK signaling
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IFITM3 promotes hepatocellular carcinoma invasion and metastasis by regulating MMP9 through p38/MAPK signaling

机译：IFITM3通过p38 / MAPK信号通路调节MMP9促进肝癌的侵袭和转移

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Interferon‐induced transmembrane protein 3 (IFITM3) has been shown to be overexpressed in multiple cancers. However, the role of IFITM3 in metastasis of hepatocellular carcinoma (HCC) is still poorly understood. In this study, we showed that IFITM3 was frequently overexpressed in HCC tissues compared with adjacent nontumor tissues. Overexpression of IFITM3 was significantly correlated with tumor metastasis and poor prognosis in HCC. Knockdown of IFITM3 dramatically decreased MMP9 expression and inhibited the invasion and metastasis of HCC in?vitro and in?vivo . Moreover, the upregulation of MMP9 rescued the decreased migration and invasion induced by the knockdown of IFITM3, whereas the knockdown of MMP9 decreased IFITM3‐enhanced HCC migration and invasion. Mechanistically, we found that IFITM3 regulates MMP9 expression through the p38/MAPK pathway. Taken together, we identified a novel IFITM3–p38/MAPK–MMP9 regulatory circuitry, the dysfunction of which drives invasive and metastatic character in HCC.
机译：干扰素诱导的跨膜蛋白3（IFITM3）已在多种癌症中过表达。然而，IFITM3在肝细胞癌（HCC）转移中的作用仍知之甚少。在这项研究中，我们表明与邻近的非肿瘤组织相比，IFITM3在HCC组织中经常过表达。 IFITM3的过表达与HCC的肿瘤转移和不良预后密切相关。抑制IFITM3可以显着降低MMP9的表达，并抑制HCC在体外和体内的侵袭和转移。此外，MMP9的上调挽救了由IFITM3敲低引起的迁移和侵袭的减少，而MMP9的敲低则降低了IFITM3增强的HCC迁移和侵袭的能力。从机制上讲，我们发现IFITM3通过p38 / MAPK途径调节MMP9表达。综上所述，我们确定了一种新型的IFITM3–p38 / MAPK–MMP9调节电路，其功能障碍会驱动HCC的侵袭和转移特性。

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