PMID- 11156403
OWN - NLM
STAT- MEDLINE
DCOM- 20010222
LR  - 20171116
IS  - 0008-5472 (Print)
IS  - 0008-5472 (Linking)
VI  - 60
IP  - 24
DP  - 2000 Dec 15
TI  - Natural killer cell-dependent suppression of systemic spread of human lung 
      adenocarcinoma cells by monocyte chemoattractant protein-1 gene transfection in 
      severe combined immunodeficient mice.
PG  - 7002-7
AB  - Monocyte chemoattractant protein-1 (MCP-1) is a chemokine with various biological 
      activities, including augmentation of cytotoxic activity of monocytes and natural 
      killer (NK) cells. The present study was undertaken to determine whether 
      transfection of the MCP-1 gene into lung cancer cells affected their 
      tumorigenicity and metastatic potential by the NK cell-mediated mechanism. The 
      human MCP-1 gene inserted into an expression vector (BCMGSNeo) was transfected 
      into human lung adenocarcinoma (PC-14) cells. There was no difference in in vitro 
      proliferation between MCP-1 gene-transfected PC-14 cells and the parent cells or 
      mock-transfected cells. The tumorigenicity and in vivo tumor growth of MCP-1 
      gene-transfected PC-14 cells were similar to those of the parent cells or 
      mock-transfected cells when tumor cells were injected into the s.c. space of NK 
      cell-intact severe combined immunodeficient (SCID) mice. Although parent cells 
      and mock-transfected cells inoculated i.v. formed lung metastatic colonies and 
      pleural effusion, MCP-1 gene transfectants reduced the systemic spread in NK 
      cell-intact SCID mice. Interestingly, these modulations in a systemic spread by 
      MCP-1 gene transfection were not observed in NK cell-depleted SCID mice. 
      Decreased survival of MCP-1 gene transfectants in the lung was observed in NK 
      cell-intact SCID mice but not in NK cell-depleted SCID mice. Recombinant MCP-1 or 
      the supernatant of MCP-1 gene transfectants enhanced the cytotoxicity of human 
      CD56+ NK cells and spleen cells of SCID mice against PC-14 cells. These findings 
      suggest that locally produced MCP-1 suppresses tumor progression by a NK 
      cell-mediated mechanism, depending on organ microenvironment.
FAU - Nokihara, H
AU  - Nokihara H
AD  - Third Department of Internal Medicine, University of Tokushima School of 
      Medicine, Japan.
FAU - Yanagawa, H
AU  - Yanagawa H
FAU - Nishioka, Y
AU  - Nishioka Y
FAU - Yano, S
AU  - Yano S
FAU - Mukaida, N
AU  - Mukaida N
FAU - Matsushima, K
AU  - Matsushima K
FAU - Sone, S
AU  - Sone S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer Res
JT  - Cancer research
JID - 2984705R
RN  - 0 (CD56 Antigen)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Recombinant Proteins)
SB  - IM
MH  - Adenocarcinoma/*immunology
MH  - Animals
MH  - Blotting, Northern
MH  - CD56 Antigen/metabolism
MH  - Cell Division/drug effects
MH  - Chemokine CCL2/*genetics
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Flow Cytometry
MH  - Genetic Vectors
MH  - Humans
MH  - Killer Cells, Natural/*drug effects/*immunology
MH  - Lung Neoplasms/*immunology
MH  - Male
MH  - Mice
MH  - Mice, SCID
MH  - Neoplasm Invasiveness
MH  - Neoplasm Transplantation
MH  - Recombinant Proteins/metabolism
MH  - Spleen/cytology
MH  - Time Factors
MH  - Transfection
MH  - Tumor Cells, Cultured
EDAT- 2001/01/13 11:00
MHDA- 2001/03/03 10:01
CRDT- 2001/01/13 11:00
PHST- 2001/01/13 11:00 [pubmed]
PHST- 2001/03/03 10:01 [medline]
PHST- 2001/01/13 11:00 [entrez]
PST - ppublish
SO  - Cancer Res. 2000 Dec 15;60(24):7002-7.