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BibTeX
Activation of the c-Met Pathway Mobilizes an Inflammatory Network in the Brain Microenvironment to Promote Brain Metastasis of Breast Cancer
Cancer research (Chicago, Ill.), 2016-09, Vol.76 (17), p.4970-4980
Xing, Fei
Liu, Yin
Sharma, Sambad
Wu, Kerui
Chan, Michael D
Lo, Hui-Wen
Carpenter, Richard L
Metheny-Barlow, Linda J
Zhou, Xiaobo
Qasem, Shadi A
Pasche, Boris
Watabe, Kounosuke
2016
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Xing, Fei
Liu, Yin
Sharma, Sambad
Wu, Kerui
Chan, Michael D
Lo, Hui-Wen
Carpenter, Richard L
Metheny-Barlow, Linda J
Zhou, Xiaobo
Qasem, Shadi A
Pasche, Boris
Watabe, Kounosuke
Titel
Activation of the c-Met Pathway Mobilizes an Inflammatory Network in the Brain Microenvironment to Promote Brain Metastasis of Breast Cancer
Ist Teil von
Cancer research (Chicago, Ill.), 2016-09, Vol.76 (17), p.4970-4980
Ort / Verlag
United States
Erscheinungsjahr
2016
Quelle
MEDLINE
Beschreibungen/Notizen
Brain metastasis is one of the chief causes of mortality in breast cancer patients, but the mechanisms that drive this process remain poorly understood. Here, we report that brain metastatic cells expressing high levels of c-Met promote the metastatic process via inflammatory cytokine upregulation and vascular reprogramming. Activated c-Met signaling promoted adhesion of tumor cells to brain endothelial cells and enhanced neovascularization by inducing the secretion of IL8 and CXCL1. Additionally, stimulation of IL1β secretion by activation of c-Met induced tumor-associated astrocytes to secrete the c-Met ligand HGF. Thus, a feed-forward mechanism of cytokine release initiated and sustained by c-Met fed a vicious cycle that generated a favorable microenvironment for metastatic cells. Reinforcing our results, we found that pterostilbene, a compound that penetrates the blood-brain barrier, could suppress brain metastasis by targeting c-Met signaling. These findings suggest a potential utility of this natural compound for chemoprevention. Cancer Res; 76(17); 4970-80. ©2016 AACR.
Sprache
Englisch
Identifikatoren
ISSN: 0008-5472
eISSN: 1538-7445
DOI: 10.1158/0008-5472.can-15-3541
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5010459
Format
–
Schlagworte
Animals
,
Antineoplastic Agents - pharmacology
,
Brain Neoplasms - secondary
,
Breast Neoplasms - pathology
,
Cell Adhesion - physiology
,
Cell Line, Tumor
,
Female
,
Heterografts
,
Humans
,
Inflammation - metabolism
,
Inflammation - pathology
,
Mice
,
Mice, Nude
,
Neoplasm Invasiveness - pathology
,
Neovascularization, Pathologic - metabolism
,
Neovascularization, Pathologic - pathology
,
Proto-Oncogene Proteins c-met - metabolism
,
Signal Transduction - physiology
,
Stilbenes - pharmacology
,
Transcriptome
,
Tumor Microenvironment - physiology
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