期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 288, 期 44, 页码 31488-31495出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M113.499020
关键词
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资金
- National Institutes of Health from NCI [2R01CA109035, 1R0CA169603]
- MD Anderson Cancer Center Support Grant [CA016672]
- Cancer Prevention and Research Institute of Texas Research [RP110252, RP130389]
- American Cancer Society Research Scholar Grant [RSG-09-277-01-CSM]
- James S. McDonnell Foundation 21st Century Science Initiative in Brain Cancer Research Award [220020318]
- Sister Institution Network Fund grants from the MDAnderson Cancer Center
- Cancer Institute and Hospital of Chinese Academy of Medical Sciences
Activated EGF receptor (EGFR) signaling plays an instrumental role in glioblastoma (GBM) progression. However, how EGFR activation regulates the tumor microenvironment to promote GBM cell invasion remains to be clarified. Here, we demonstrate that the levels of EGFR activation in tumor cells correlated with the levels of macrophage infiltration in human GBM specimens. This was supported by our observation that EGFR activation enhanced the interaction between macrophages and GBM cells. In addition, EGF treatment induced up-regulation of vascular cell adhesion molecule-1 (VCAM-1) expression in a PKC epsilon- and NF-kappa B-dependent manner. Depletion of VCAM-1 interrupted the binding of macrophages to GBM cells and inhibited EGF-induced and macrophage-promoted GBM cell invasion. These results demonstrate an instrumental role for EGF-induced up-regulation of VCAM-1 expression in EGFR activation-promoted macrophage-tumor cell interaction and tumor cell invasion and indicate that VCAM-1 is a potential molecular target for improving cancer therapy.
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