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首页> 外文期刊>Journal of cellular physiology. >Glycochenodeoxycholate promotes the metastasis of gallbladder cancer cells by inducingepithelial to mesenchymal transition via activation of SOCS3/JAK2/STAT3 signaling pathway
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Glycochenodeoxycholate promotes the metastasis of gallbladder cancer cells by inducingepithelial to mesenchymal transition via activation of SOCS3/JAK2/STAT3 signaling pathway

机译：Glycochenodeoxycholate促进转移的通过inducingepithelial胆囊癌症细胞通过激活间充质转变SOCS3 / JAK2 / STAT3信号通路

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摘要

The incidence of gallbladder cancer (GBC) is relatively rare but a high degree of malignancy. The migration and invasion potential of GBC severely affects the prognosis of patients with GBC. Glycochenodeoxycholate (GCDC) is one of the most important components in GBC-associated microenvironment. However, the role of GCDC in the metastatic feature of GBC cells is not fully understood. First, the results of this study found that GCDC could effectively enhance the metastasis of GBC cells. Furthermore, GCDC could lead to the enhancement of epithelial to mesenchymal transition (EMT) phenotype in GBC cells, which is concerned to be an important mechanism of tumor metastasis. Further studies showed that GCDC treatment induced the upregulation of matrix metalloproteinase-3 (MMP3), MMP9, and SOCS3/ JAK2/p-STAT3 signal pathway in GBC cells, which could regulate the level of EMT. Beside that, we also found the positive expression of farnesoid X receptor (FXR) in GBC cells and inhibition of FXR could significantly block the effect of GCDC on the metastasis of GBC cells. These results indicated that GCDC promoted GBC cells metastasis by enhancing the level of EMT and inhibition of FXR could significantly block the effect of GCDC. On one hand, FXR might be an indicator for predicting the metastasis of patient with GBC. On the other hand, FXR might serve as a potential antimetastasis target in GBC therapy.
机译：胆囊癌症的发病率(GBC)相对少见,但高度恶性肿瘤。GBC的迁移和入侵潜力严重影响患者的预后GBC。在GBC-associated最重要的组件微环境。GBC细胞的转移特性并不完全理解。发现GCDC可以有效地提高GBC细胞的转移。导致上皮的增强间充质转变(EMT) GBC的表型而言是一个重要的细胞肿瘤转移机制。表明GCDC治疗诱导upregulation矩阵metalloproteinase-3(MMP3)、MMP9 SOCS3 JAK2 / p-STAT3信号GBC细胞通路,可以调节EMT的水平。积极表达farnesoid X受体(FXR)GBC细胞和抑制FXR大大块GCDC在的效果GBC细胞的转移。GCDC提升GBC细胞转移加强EMT的水平和FXR的抑制可能大大块GCDC的效果。一方面,FXR可能是一个指标预测GBC患者的转移。另一方面,FXR可能作为一个潜在的antimetastasis GBC治疗目标。

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