PMID- 24953854
OWN - NLM
STAT- MEDLINE
DCOM- 20150409
LR  - 20171116
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 21
IP  - 2
DP  - 2014 Aug
TI  - Dexamethasone inhibits in vivo tumor growth by the alteration of bone marrow 
      CD11b(+) myeloid cells.
PG  - 494-500
LID - S1567-5769(14)00220-3 [pii]
LID - 10.1016/j.intimp.2014.06.006 [doi]
AB  - Inflammation is closely associated with tumor growth, which is mediated by the 
      activation of bone marrow-derived CD11b(+) cells. Here, we investigated whether 
      anti-inflammatory dexamethasone (Dex), a synthetic glucocorticoid (GC), could 
      regulate tumor growth and CD11b(+) myeloid bone marrow cells (BMCs) in lymphocyte 
      (R1), monocyte (R2) and granulocyte (R3) regions of FSC-SSC dot plot. The growth 
      of B16F10 mouse melanoma tumor was inhibited in Dex-injected group. Lung 
      metastasis was decreased and the lifespan was elongated in Dex-injected mice with 
      tumor resection. Intravenous injection of B16F10 cells increased the percentage 
      of CD11b(+) myeloid BMCs in R1 and R2 regions from 3h to 72h. In contrast, little 
      changes in the percentage of CD11b(+) myeloid BMCs were detected in R3 region. 
      Among CD11b(+) myeloid BMCs, the percentage of CD11b(+)Gr-1(+) cells was 
      increased in R1, R2 and R3 regions. Absolute number of CD11b(+) and 
      CD11b(+)Gr-1(+) cells was enhanced in R1 region from 3h to 72 h. B16F10 tumor 
      growth was significantly increased by intravenous injection of CD11b(+) BMCs. 
      Tumor-bearing mice showed an increase in the percentage of CD11b(+) myeloid BMCs 
      in R2 region and CD11b(+)Gr-1(+) cells in R2 and R3 regions, which are reduced by 
      intravenous injection with Dex. Absolute number of CD11b(+)Gr-1(+) cells was 
      enhanced in R2 and R3 regions. Tumor growth was significantly inhibited by 
      intravenous injection of BMCs collected from Dex-treated tumor-bearing mice. 
      Taken together, data demonstrate that tumor regression by Dex was resulted from 
      the alteration of CD11b(+) myeloid BMCs and their inhibitory function to tumor 
      growth. It suggests that CD11b(+) myeloid BMCs could regulate antitumor efficacy 
      of GCs such as Dex.
CI  - Copyright (c) 2014 Elsevier B.V. All rights reserved.
FAU - Moon, Eun-Yi
AU  - Moon EY
AD  - Department of Bioscience and Biotechnology, Sejong University, Seoul 143-747, 
      Republic of Korea. Electronic address: eunyimoon@sejong.ac.kr.
FAU - Ryu, Yun-Kyoung
AU  - Ryu YK
AD  - Department of Bioscience and Biotechnology, Sejong University, Seoul 143-747, 
      Republic of Korea.
FAU - Lee, Geun-Hee
AU  - Lee GH
AD  - Department of Bioscience and Biotechnology, Sejong University, Seoul 143-747, 
      Republic of Korea.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140619
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (CD11b Antigen)
RN  - 0 (Gr-1 protein, mouse)
RN  - 0 (Receptors, Chemokine)
RN  - 7S5I7G3JQL (Dexamethasone)
SB  - IM
EIN - Int Immunopharmacol. 2014 Oct;22(2):526-7
MH  - Animals
MH  - Anti-Inflammatory Agents/pharmacology
MH  - Bone Marrow/*drug effects/metabolism
MH  - Bone Marrow Cells/*drug effects/metabolism
MH  - CD11b Antigen/*metabolism
MH  - Dexamethasone/*pharmacology
MH  - Female
MH  - Granulocytes/drug effects/metabolism
MH  - Lymphocytes/drug effects/metabolism
MH  - Melanoma, Experimental/diet therapy/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Monocytes/drug effects/metabolism
MH  - Myeloid Cells/*drug effects/metabolism
MH  - Receptors, Chemokine/metabolism
OTO - NOTNLM
OT  - Bone marrow cells
OT  - CD11b(+)
OT  - CD11b(+)Gr-1(+)
OT  - Dexamethasone
OT  - MDSC
OT  - Tumor growth
EDAT- 2014/06/24 06:00
MHDA- 2015/04/10 06:00
CRDT- 2014/06/24 06:00
PHST- 2014/02/09 00:00 [received]
PHST- 2014/05/28 00:00 [revised]
PHST- 2014/06/04 00:00 [accepted]
PHST- 2014/06/24 06:00 [entrez]
PHST- 2014/06/24 06:00 [pubmed]
PHST- 2015/04/10 06:00 [medline]
AID - S1567-5769(14)00220-3 [pii]
AID - 10.1016/j.intimp.2014.06.006 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2014 Aug;21(2):494-500. doi: 10.1016/j.intimp.2014.06.006. 
      Epub 2014 Jun 19.