CXCL5型
上皮-间质转换
PI3K/AKT/mTOR通路
蛋白激酶B
癌症研究
趋化因子受体
蜗牛
信号转导
生物
转移
医学
内科学
免疫学
趋化因子
细胞生物学
癌症
趋化因子受体
生态学
免疫系统
作者
Shao‐Lai Zhou,Zheng‐Jun Zhou,Zhiqiang Hu,Xun Li,Xiaowu Huang,Zheng Wang,Jia Fan,Zhi Dai,Jian Zhou
出处
期刊:Cancer Letters
[Elsevier]
日期:2014-11-24
卷期号:358 (2): 124-135
被引量:165
标识
DOI:10.1016/j.canlet.2014.11.044
摘要
Upregulation of CXCR2 in tumor cells has been documented in several types of cancer. As one of its ligands, CXCL5 is associated with neutrophil infiltration and poor prognosis in hepatocellular carcinoma (HCC). However, little is known about the role of the CXCR2/CXCL5 axis in the invasion and metastasis of HCC cells. In this study, we examined CXCR2 expression in human HCC cell lines and in three independent cohorts of HCC patients. The molecular effects of high expression levels of CXCR2 and CXCL5 in HCC cells were determined using qRT-PCR, western blot analysis, immunofluorescence, matrigel invasion assay, and xenograft mouse models. We found that high levels of CXCR2 correlated with progression and poor prognosis in human HCC. CXCR2/CXCL5 together promoted cell spreading by inducing the epithelial-mesenchymal transition (EMT) through activation of the PI3K/Akt/GSK-3β/Snail signaling pathway. In clinical HCC samples, high expression of both CXCR2 and CXCL5 showed a significant correlation with the activation of PI3K/Akt/GSK-3β/Snail signaling and EMT phenotype. In conclusion, our data showed that the CXCR2/CXCL5 axis contributes to EMT of HCC cells through activating PI3K/Akt/GSK-3β/Snail signaling, and it may serve as a potential therapeutic target.
科研通智能强力驱动
Strongly Powered by AbleSci AI