Document Detail

S1PR1-STAT3 signaling is crucial for myeloid cell colonization at future metastatic sites.
MedLine Citation:
PMID:  22624714     Owner:  NLM     Status:  MEDLINE    
Recent studies underscore the importance of myeloid cells in rendering distant organs hospitable for disseminating tumor cells to colonize. However, what enables myeloid cells to have an apparently superior capacity to colonize distant organs is unclear. Here, we show that S1PR1-STAT3 upregulation in tumor cells induces factors that activate S1PR1-STAT3 in various cells in premetastatic sites, leading to premetastatic niche formation. Targeting either S1PR1 or STAT3 in myeloid cells disrupts existing premetastatic niches. S1PR1-STAT3 pathway enables myeloid cells to intravasate, prime the distant organ microenvironment and mediate sustained proliferation and survival of their own and other stromal cells at future metastatic sites. Analyzing tumor-free lymph nodes from cancer patients shows elevated myeloid infiltrates, STAT3 activity, and increased survival signal.
Jiehui Deng; Yong Liu; Heehyoung Lee; Andreas Herrmann; Wang Zhang; Chunyan Zhang; Shudan Shen; Saul J Priceman; Maciej Kujawski; Sumanta K Pal; Andrew Raubitschek; Dave S B Hoon; Stephen Forman; Robert A Figlin; Jie Liu; Richard Jove; Hua Yu
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Video-Audio Media    
Journal Detail:
Title:  Cancer cell     Volume:  21     ISSN:  1878-3686     ISO Abbreviation:  Cancer Cell     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-05-25     Completed Date:  2012-07-26     Revised Date:  2014-09-12    
Medline Journal Info:
Nlm Unique ID:  101130617     Medline TA:  Cancer Cell     Country:  United States    
Other Details:
Languages:  eng     Pagination:  642-54     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Inc. All rights reserved.
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MeSH Terms
Cell Line, Tumor
Cell Movement
Cell Proliferation
Cell Survival
CpG Islands
Lung Neoplasms / metabolism,  secondary
Lymph Nodes / metabolism,  pathology
Lymphatic Metastasis
Melanoma / metabolism,  secondary
Mice, Knockout
Myeloid Cells / metabolism*,  pathology
Neoplasm Invasiveness
Neoplasms / metabolism*,  pathology*
Prostatic Neoplasms / genetics,  metabolism*,  pathology
RNA Interference
Receptors, Lysosphingolipid / deficiency,  genetics,  metabolism*
STAT3 Transcription Factor / deficiency,  genetics,  metabolism*
Signal Transduction*
Skin Neoplasms / metabolism,  pathology
Time Factors
Transduction, Genetic
Tumor Microenvironment*
Urinary Bladder Neoplasms / metabolism,  pathology
Grant Support
2K12CA001727-16A1/CA/NCI NIH HHS; P30 CA33572/CA/NCI NIH HHS; P50 CA107399/CA/NCI NIH HHS; P50 CA107399-06A1/CA/NCI NIH HHS; P50 CA107399-07/CA/NCI NIH HHS; R01 CA115674/CA/NCI NIH HHS; R01 CA115815/CA/NCI NIH HHS; R01 CA115815/CA/NCI NIH HHS; R01 CA115815-05/CA/NCI NIH HHS; R01 CA122976/CA/NCI NIH HHS; R01 CA122976/CA/NCI NIH HHS; R01 CA122976-04/CA/NCI NIH HHS; R01 CA122976-05/CA/NCI NIH HHS; R01 CA122976-06/CA/NCI NIH HHS; R01 CA140692/CA/NCI NIH HHS
Reg. No./Substance:
0/Receptors, Lysosphingolipid; 0/S1PR1 protein, human; 0/S1pr1 protein, mouse; 0/STAT3 Transcription Factor; 0/STAT3 protein, human; 0/Stat3 protein, mouse

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