上皮-间质转换
转移
癌症研究
STAT蛋白
车站3
肝细胞癌
转化生长因子
磷酸化
细胞迁移
生物
化学
体外
细胞生物学
生物化学
癌症
遗传学
作者
Jie Mo,Zhaoqi Zhang,Ning Deng,Qiumeng Liu,Chao Wang,Qianyun Ge,Peng-Chen Du,Shasha Song,Xuewu Zhang,Long-Xin,Huifang Liang,Liang Chu,Lei Zhang,Xiaoping Chen,Jin Chen,Hanhua Dong,Bixiang Zhang
标识
DOI:10.1142/s0192415x22500124
摘要
18[Formula: see text]-glycyrrhetinic acid (GA) is the active ingredient of the traditional Chinese medicinal herb Glycyrrhizae radix et rhizoma. We previously demonstrated that GA inhibited tumor growth in hepatocellular carcinoma (HCC). However, the effect of GA on transforming growth factor-[Formula: see text] (TGF-[Formula: see text]-induced epithelial-mesenchymal transition (EMT) and metastasis were still unclear. In this study, in vitro transwell assays and immunofluorescence (IF) demonstrated that GA inhibited TGF-[Formula: see text]-induced migration, invasion and EMT of HCC cells. However, it had little effect on the inhibition of proliferation by TGF-[Formula: see text]. Moreover, we confirmed that GA suppressed the metastasis of HCC cells in vivousing an ectopic lung metastasis model. Furthermore, we found that GA inhibited TGF-[Formula: see text]-induced EMT mainly by reducing the phosphorylation of signal transducer and activator of transcription 3 (STAT3), which played an essential role in TGF-[Formula: see text]-induced EMT and cell mobility. Mechanistically, GA inhibited the phosphorylation of STAT3 by increasing the expression of Src homology 2 domain-containing protein tyrosine phosphatases 1 and 2 (SHP1 and SHP2). Therefore, we concluded that GA inhibited TGF-[Formula: see text]-induced EMT and metastasis via the SHP1&SHP2/STAT3/Snail pathway. Our data provide an attractive therapeutic target for future multimodal management of HCC.
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