PMID- 24384681
OWN - NLM
STAT- MEDLINE
DCOM- 20140407
LR  - 20211021
IS  - 1532-1827 (Electronic)
IS  - 0007-0920 (Print)
IS  - 0007-0920 (Linking)
VI  - 110
IP  - 3
DP  - 2014 Feb 4
TI  - Circulating galectins -2, -4 and -8 in cancer patients make important 
      contributions to the increased circulation of several cytokines and chemokines 
      that promote angiogenesis and metastasis.
PG  - 741-52
LID - 10.1038/bjc.2013.793 [doi]
AB  - BACKGROUND: Circulating concentrations of the cytokines interleukin-6 (IL-6), 
      granulocyte colony-stimulating factor (G-CSF) and chemokines monocyte chemotatic 
      protein 1 (MCP-1)/CCL2 and growth-regulator oncogene alpha (GROalpha)/chemokine C-X-C 
      motif ligand 1 are commonly increased in cancer patients and they are 
      increasingly recognised as important promoters, via divergent mechanisms, of 
      cancer progression and metastasis. METHODS: The effect of galectins-2, -4 and -8, 
      whose circulating levels are highly increased in cancer patients, on endothelial 
      secretion of cytokines was assessed in vitro by cytokine array and in mice. The 
      relationship between serum levels of galectins and cytokines was analysed in 
      colon and breast cancer patients. RESULTS: Galectins-2, -4 and -8 at pathological 
      concentrations induce secretion of G-CSF, IL-6, MCP-1 and GROalpha from the blood 
      vascular endothelial cells in vitro and in mice. Multiple regression analysis 
      indicates that increased circulation of these galectins accounts for 41 approximately 83% of 
      the variance of these cytokines in the sera of colon and breast cancer patients. 
      The galectin-induced secretion of these cytokines/chemokines is shown to enhance 
      the expression of endothelial cell surface adhesion molecules, causing increased 
      cancer-endothelial adhesion and increased endothelial tubule formation. 
      CONCLUSION: The increased circulation of galectins -2, -4 and -8 in cancer 
      patients contributes substantially to the increased circulation of G-CSF, IL-6 
      and MCP-1 by interaction with the blood vascular endothelium. These cytokines and 
      chemokines in turn enhance endothelial cell activities in angiogenesis and 
      metastasis.
FAU - Chen, C
AU  - Chen C
AD  - Department of Gastroenterology, Institute of Translational Medicine, University 
      of Liverpool, Liverpool, UK.
FAU - Duckworth, C A
AU  - Duckworth CA
AD  - Department of Gastroenterology, Institute of Translational Medicine, University 
      of Liverpool, Liverpool, UK.
FAU - Fu, B
AU  - Fu B
AD  - Institute of Population Health, University of Manchester, Manchester, UK.
FAU - Pritchard, D M
AU  - Pritchard DM
AD  - Institute of Population Health, University of Manchester, Manchester, UK.
FAU - Rhodes, J M
AU  - Rhodes JM
AD  - Institute of Population Health, University of Manchester, Manchester, UK.
FAU - Yu, L-G
AU  - Yu LG
AD  - Institute of Population Health, University of Manchester, Manchester, UK.
LA  - eng
GR  - G1000772/Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140102
PL  - England
TA  - Br J Cancer
JT  - British journal of cancer
JID - 0370635
RN  - 0 (CCL2 protein, human)
RN  - 0 (CXCL1 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CXCL1)
RN  - 0 (Galectin 2)
RN  - 0 (Galectin 4)
RN  - 0 (Galectins)
RN  - 0 (Interleukin-6)
RN  - 0 (LGALS8 protein, human)
RN  - 143011-72-7 (Granulocyte Colony-Stimulating Factor)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/metabolism
MH  - Chemokine CXCL1/metabolism
MH  - Galectin 2/*blood
MH  - Galectin 4/*blood
MH  - Galectins/*blood
MH  - Granulocyte Colony-Stimulating Factor/metabolism
MH  - Humans
MH  - Interleukin-6/genetics
MH  - Mice
MH  - Neoplasm Metastasis/pathology
MH  - Neoplasms/blood/genetics
MH  - Neoplastic Cells, Circulating
MH  - Neovascularization, Pathologic/blood/*genetics
PMC - PMC3915140
EDAT- 2014/01/05 06:00
MHDA- 2014/04/08 06:00
PMCR- 2015/02/04
CRDT- 2014/01/04 06:00
PHST- 2013/09/17 00:00 [received]
PHST- 2013/11/17 00:00 [revised]
PHST- 2013/11/21 00:00 [accepted]
PHST- 2014/01/04 06:00 [entrez]
PHST- 2014/01/05 06:00 [pubmed]
PHST- 2014/04/08 06:00 [medline]
PHST- 2015/02/04 00:00 [pmc-release]
AID - bjc2013793 [pii]
AID - 10.1038/bjc.2013.793 [doi]
PST - ppublish
SO  - Br J Cancer. 2014 Feb 4;110(3):741-52. doi: 10.1038/bjc.2013.793. Epub 2014 Jan 
      2.