PMID- 21463547
OWN - NLM
STAT- MEDLINE
DCOM- 20110722
LR  - 20191112
IS  - 1488-2353 (Electronic)
IS  - 0147-958X (Linking)
VI  - 34
IP  - 2
DP  - 2011 Apr 1
TI  - N-glycan-defective breast cancer cells induce a phenotypic switch in polarization 
      of bone marrow-derived macrophages.
PG  - E71-81
AB  - PURPOSE: To investigate the effect of N-glycan-defective mammary adenocarcinoma 
      cells on the polarization of macrophages. METHODS: N-glycan-defective breast 
      cancer cells (MA782 cells) were prepared by swainsonine (SW) treatment and the 
      cytotoxicity of SW to MA782 cells was evaluated using the 
      3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay. The 
      N-glycan-defective MA782 cells were co-cultured with bone marrow-derived 
      macrophages (BMDMs) for 48 h in vitro, and then the BMDMs and the co-cultured 
      supernatant were analyzed for macrophage phenotypic using FQRT-PCR, FCM and 
      ELISA. RESULTS: SW-treated MA782 cells expressed defective N-glycan on the cell 
      surface in a dose-dependent manner (*p < 0.05). MTT assays showed that neither 
      the 1 mug/mL nor 5 mug/mL SW treatments showed significant inhibition of MA782 cell 
      growth in vitro. The expression of iNOS and agr-1 in the 5 mug/mL SW-treated group 
      were 4.75-fold higher and 3.7-fold lower than that in the untreated group, 
      respectively (*p < 0.05). Mean fluorescence intensity of CD16/32 expressed in the 
      cells treated with 5 mug/mL SW was significantly higher in comparison with the 
      untreated group (65 vs. 7, *p < 0.05), though the percentage of CD16/32-positive 
      cells were not significantly different. Furthermore, the expression of CD206 and 
      dectin-1 in the 5 mug/mL SW-treated group was significantly decreased (3.1+/-0.3% 
      and 4.1+/-1.1%, respectively) in comparison with the untreated group (40+/-3% and 
      8.9+/-1.2%, respectively, both p < 0.05). In addition, the 5 mug/mL SW-treated group 
      secreted more TNF-alpha (350 +/-25 pg/mL) and less IL-10 (89+/-7.2 pg/mL) than the 
      untreated group (80 +/-3 pg/mL and 150 +/-10 pg/mL, respectively, both p < 0.05). 
      CONCLUSION: N-glycan-defective MA782 cells can induce the differentiation of BMDM 
      into proinflammatory M1 macrophages in vitro.
FAU - Chen, Haidan
AU  - Chen H
AD  - Department of Immunology, School of Basic Medical Science, Wuhan University, 
      Wuhan, Hubei, P.R. China.
FAU - Cai, Huili
AU  - Cai H
FAU - Chen, Liang
AU  - Chen L
FAU - Wu, Xianglei
AU  - Wu X
FAU - Li, Dongqing
AU  - Li D
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110401
PL  - Canada
TA  - Clin Invest Med
JT  - Clinical and investigative medicine. Medecine clinique et experimentale
JID - 7804071
RN  - 0 (DNA Primers)
RN  - 0 (Polysaccharides)
RN  - RSY4RK37KQ (Swainsonine)
SB  - IM
MH  - Base Sequence
MH  - Bone Marrow Cells/*cytology
MH  - Breast Neoplasms/metabolism/*pathology
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - DNA Primers
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Humans
MH  - Macrophages/*cytology
MH  - Phenotype
MH  - Polysaccharides/antagonists & inhibitors/biosynthesis/*metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Swainsonine/pharmacology
EDAT- 2011/04/06 06:00
MHDA- 2011/07/23 06:00
CRDT- 2011/04/06 06:00
PHST- 2011/04/01 00:00 [received]
PHST- 2011/04/06 06:00 [entrez]
PHST- 2011/04/06 06:00 [pubmed]
PHST- 2011/07/23 06:00 [medline]
AID - 10.25011/cim.v34i1.15103 [doi]
PST - epublish
SO  - Clin Invest Med. 2011 Apr 1;34(2):E71-81. doi: 10.25011/cim.v34i1.15103.