PMID- 22138288
OWN - NLM
STAT- MEDLINE
DCOM- 20120214
LR  - 20220309
IS  - 1873-2968 (Electronic)
IS  - 0006-2952 (Linking)
VI  - 83
IP  - 3
DP  - 2012 Feb 1
TI  - CCL2 increases MMP-9 expression and cell motility in human chondrosarcoma cells 
      via the Ras/Raf/MEK/ERK/NF-kappaB signaling pathway.
PG  - 335-44
LID - 10.1016/j.bcp.2011.11.013 [doi]
AB  - Chondrosarcoma is a type of highly malignant tumor with a potent capacity to 
      invade locally and cause distant metastasis. Chondrosarcoma shows a predilection 
      for metastasis to the lungs. Chemokine ligand 2 (CCL2), also known as monocyte 
      chemoattractant protein-1 (MCP-1), belongs to the CC chemokine family that is 
      associated with the disease status and outcomes of cancers. However, the effect 
      of CCL2 on migration activity in human chondrosarcoma cells is mostly unknown. 
      Here we found that CCL2 increased the migration and expression of matrix 
      metalloproteinase (MMP)-9 in human chondrosarcoma cells. CCL2-mediated migration 
      and MMP-9 up-regulation were attenuated by CCR2, Ras, Raf-1, and MEK inhibitor. 
      Activation of the Ras, Raf-1, MEK, ERK, and NF-kappaB signaling pathway after CCL2 
      treatment was demonstrated, and CCL2-induced expression of MMP-9 and migration 
      activity were inhibited by the specific inhibitor, and mutant of Ras, Raf-1, MEK, 
      ERK, and NF-kappaB cascades. Taken together, our results indicated that CCL2 enhances 
      the migration of chondrosarcoma cells by increasing MMP-9 expression through the 
      CCR2 receptor, Ras, Raf-1, MEK, ERK, and NF-kappaB signal transduction pathway.
CI  - Copyright (c) 2011 Elsevier Inc. All rights reserved.
FAU - Tang, Chih-Hsin
AU  - Tang CH
AD  - Department of Pharmacology, School of Medicine, China Medical University, 
      Taichung, Taiwan. chtang@mail.cmu.edu.tw
FAU - Tsai, Chia-Chun
AU  - Tsai CC
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20111125
PL  - England
TA  - Biochem Pharmacol
JT  - Biochemical pharmacology
JID - 0101032
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (Receptors, CCR2)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-raf)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
RN  - EC 3.6.5.2 (ras Proteins)
SB  - IM
MH  - Bone Neoplasms/enzymology/*metabolism/pathology
MH  - Cell Line, Tumor
MH  - Cell Movement/drug effects/*physiology
MH  - Chemokine CCL2/*physiology
MH  - Chondrosarcoma/enzymology/*metabolism/pathology
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - MAP Kinase Signaling System/drug effects/*physiology
MH  - Matrix Metalloproteinase 9/*biosynthesis
MH  - NF-kappa B/*physiology
MH  - Proto-Oncogene Proteins c-raf/physiology
MH  - Receptors, CCR2/physiology
MH  - ras Proteins/*physiology
EDAT- 2011/12/06 06:00
MHDA- 2012/02/15 06:00
CRDT- 2011/12/06 06:00
PHST- 2011/10/05 00:00 [received]
PHST- 2011/11/15 00:00 [revised]
PHST- 2011/11/16 00:00 [accepted]
PHST- 2011/12/06 06:00 [entrez]
PHST- 2011/12/06 06:00 [pubmed]
PHST- 2012/02/15 06:00 [medline]
AID - S0006-2952(11)00850-1 [pii]
AID - 10.1016/j.bcp.2011.11.013 [doi]
PST - ppublish
SO  - Biochem Pharmacol. 2012 Feb 1;83(3):335-44. doi: 10.1016/j.bcp.2011.11.013. Epub 
      2011 Nov 25.