PMID- 9258345
OWN - NLM
STAT- MEDLINE
DCOM- 19970911
LR  - 20081121
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 172
IP  - 2
DP  - 1997 Aug
TI  - Moloney murine leukemia virus long terminal repeat activates monocyte chemotactic 
      protein-1 protein expression and chemotactic activity.
PG  - 240-52
AB  - Moloney murine leukemia virus (Mo-MuLV) is a thymotropic and leukemogenic 
      retrovirus which causes T lymphomas. Recently, Mo-MuLV has been shown to 
      trans-activate cellular genes. Monocyte chemoattractant protein-1 (MCP-1) is a 
      chemokine which can promote the migration and diapedesis of monocytes and 
      lymphocytes, as well as inducing metastasis of lymphomas. Here we demonstrate 
      that introduction of Mo-MuLV or the MuLV LTR alone, transiently or stably, into 
      Balb/c-3T3 cells or HeLa cells resulted in 9-11 fold increases in MCP-1 
      transcripts. This trans-activation of the MCP-1 gene by the Mo-MuLV LTR is 
      independent of the physical location of the MCP-1 gene or of the LTR, occurring 
      whether the LTR or the MCP-1 gene is integrated in the genome or transiently 
      expressed. Immunoblot analysis using an anti-MCP-1 polyclonal antibody showed 
      that the expression of the MuLV LTR in HeLa cells also induced the appearance of 
      the MCP-1 protein. Boyden Chamber analysis demonstrated that the MCP-1 
      chemotactic activity produced by HeLa cells with an integrated MuLV LTR was 
      elevated by 11 fold and that neutralizing antibody to human MCP-1 abrogated 
      monocyte migration in response to MuLV LTR expression. Promoter deletional 
      analysis showed the LTR responsive cis-acting element in the MCP-1 promoter is 
      located between -141 and -88. Deletion of this region abolished the 
      trans-activation of MCP-1 by the LTR. These LTR-mediated activations of a 
      chemotactic and inflammatory cytokine may be relevant as mechanisms whereby 
      retroviruses which do not contain oncogenes can induce neoplasia.
FAU - Faller, D V
AU  - Faller DV
AD  - Cancer Research Center, Boston University School of Medicine, Massachusetts 
      02118, USA. dfaller@bu.edu
FAU - Weng, H
AU  - Weng H
FAU - Graves, D T
AU  - Graves DT
FAU - Choi, S Y
AU  - Choi SY
LA  - eng
GR  - CA-65420/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/genetics/*metabolism
MH  - *Chemotaxis, Leukocyte
MH  - HeLa Cells
MH  - Humans
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Moloney murine leukemia virus/*genetics
MH  - RNA, Messenger/metabolism
MH  - Repetitive Sequences, Nucleic Acid/*physiology
MH  - Transcriptional Activation
MH  - Tumor Cells, Cultured
EDAT- 1997/08/01 00:00
MHDA- 2000/06/20 09:00
CRDT- 1997/08/01 00:00
PHST- 1997/08/01 00:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1997/08/01 00:00 [entrez]
AID - 10.1002/(SICI)1097-4652(199708)172:2<240::AID-JCP11>3.0.CO;2-D [pii]
AID - 10.1002/(SICI)1097-4652(199708)172:2<240::AID-JCP11>3.0.CO;2-D [doi]
PST - ppublish
SO  - J Cell Physiol. 1997 Aug;172(2):240-52. doi: 
      10.1002/(SICI)1097-4652(199708)172:2<240::AID-JCP11>3.0.CO;2-D.