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The Effect and Mechanism of CXCR4 Silencing on Metastasis Suppression of Human Glioma U87 Cell Line
Author(s) -
Zhu Yu,
Yang Ping,
Zhang Xuebin,
Zhang Ling,
Cui Guiping,
Wang Qin,
Lv Lixia,
Zhang Yi,
Xin Xin,
Yan Tao,
Zhao Meng,
Zhang Nan
Publication year - 2013
Publication title -
the anatomical record
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.22825
Subject(s) - gene silencing , glioma , cancer research , metastasis , cd44 , pten , cell cycle , cxcr4 , u87 , protein kinase b , biology , cell , pi3k/akt/mtor pathway , phosphorylation , cancer , microbiology and biotechnology , signal transduction , immunology , gene , biochemistry , genetics , chemokine , immune system
Tumor metastasis is the major cause of treatment failure and poor prognosis of glioma. Inhibiting metastasis has become an important therapeutic strategy for glioma treatment. CXCR4 has been proved to play an important role in the occurrence and development of tumors. In order to illustrate the effect of CXCR4 on glioma metastasis, we investigated the role of CXCR4 in U87 cells metastasis based on the CXCR4 silencing tumor cells. In this study, we found that CXCR4 silencing could suppress U87 cells invasion and adhesion potential, production of TGF‐β1, IL‐6, and IL‐8, and blocked the G0/G1 phase of the cell cycle. We also found that CXCR4 silencing could up‐regulate the mRNA and protein expression of p53, p21, and E‐cadherin, and down‐regulate the mRNA and protein expression of CD44 and MMP‐2/‐9. Meanwhile, CXCR4 silencing could decrease the phosphorylation of p‐AKT and transcription activity of NF‐κB promoter, and increased the phosphorylation of PTEN. The results provided a new research basis for the further study of CXCR4 gene, the screening of human glioma, as well as the target treatment for glioma and its prognosis. Anat Rec, 296:1857–1864, 2013. © 2013 Wiley Periodicals, Inc.