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      CXCR2/CXCL5 axis contributes to epithelial-mesenchymal transition of HCC cells through activating PI3K/Akt/GSK-3β/Snail signaling.

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          Abstract

          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.

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          Author and article information

          Journal
          Cancer Lett.
          Cancer letters
          1872-7980
          0304-3835
          Mar 28 2015
          : 358
          : 2
          Affiliations
          [1 ] Liver Surgery Department, Liver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education, Fudan University, Shanghai 200032, China; Institute of Biomedical Sciences, Fudan University, Shanghai, China.
          [2 ] Liver Surgery Department, Liver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education, Fudan University, Shanghai 200032, China.
          [3 ] Liver Surgery Department, Liver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education, Fudan University, Shanghai 200032, China; Institute of Biomedical Sciences, Fudan University, Shanghai, China. Electronic address: dai.zhi@zs-hospital.sh.cn.
          [4 ] Liver Surgery Department, Liver Cancer Institute, Zhongshan Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education, Fudan University, Shanghai 200032, China; Institute of Biomedical Sciences, Fudan University, Shanghai, China. Electronic address: zhou.jian@zs-hospital.sh.cn.
          Article
          S0304-3835(14)00715-0
          10.1016/j.canlet.2014.11.044
          25462858
          b039c925-07f2-4a43-80c7-9b9d177c5575
          Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
          History

          CXCL5,CXCR2,Epithelial–mesenchymal transition,Hepatocellular carcinoma,Metastasis

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