PMID- 9139838
OWN - NLM
STAT- MEDLINE
DCOM- 19970523
LR  - 20190708
IS  - 0020-7136 (Print)
IS  - 0020-7136 (Linking)
VI  - 71
IP  - 2
DP  - 1997 Apr 10
TI  - Combined therapy of multidrug-resistant human lung cancer with 
      anti-P-glycoprotein antibody and monocyte chemoattractant protein-1 gene 
      transduction: the possibility of immunological overcoming of multidrug 
      resistance.
PG  - 170-7
AB  - We determined whether transduction of the monocyte chemoattractant protein-1 
      (MCP-1) gene into MDR human lung cancer cells affected their tumorigenicity and 
      sensitivity to antibody-dependent cellular cytotoxicity (ADCC) reaction mediated 
      by the anti-P-glycoprotein (P-gp) monoclonal antibody MRK16. The human MCP-1 gene 
      inserted into an expression vector (BCMGSNeo) was transfected into MDR human 
      small-cell lung cancer (H69/VP) cells. Monocyte chemotactic activity was found in 
      culture supernatants collected from MCP-1-transfected H69/VP cells, but not in 
      supernatants of parent and mock-transfected cells. In an in vitro experiment, 
      recombinant MCP-1 did not affect monocyte-mediated ADCC against H69/VP cells when 
      added to the monocyte culture in either the activation or the effector phase at 
      sufficient concentrations to attract and activate monocytes. Tumorigenicity and 
      growth rates of MCP-1-producing H69/VP cells in nude mice were similar to those 
      of parental cells and mock-transfected cells. However, systemic treatment with 
      MRK16 was more effective in inhibiting the formation of tumors by 
      MCP-1-gene-transfected cells than by mock-transfected cells. Systemic treatment 
      with MRK16 also inhibited the growth of a mixture (1:1) of MCP-1-producing cells 
      and mock-transfected cells. These results suggest that combination therapy with 
      MRK16 and MCP-1 gene transduction may be a useful immunological strategy to 
      inhibit the growth of human MDR cancer cells expressing P-gp.
FAU - Nishioka, Y
AU  - Nishioka Y
AD  - Third Department of Internal Medicine, The University of Tokushima School of 
      Medicine, Tokushima City, Japan.
FAU - Yano, S
AU  - Yano S
FAU - Fujiki, F
AU  - Fujiki F
FAU - Mukaida, N
AU  - Mukaida N
FAU - Matsushima, K
AU  - Matsushima K
FAU - Tsuruo, T
AU  - Tsuruo T
FAU - Sone, S
AU  - Sone S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - 0 (ATP Binding Cassette Transporter, Subfamily B, Member 1)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - ATP Binding Cassette Transporter, Subfamily B, Member 1/*immunology
MH  - Animals
MH  - Antibodies, Monoclonal/*therapeutic use
MH  - Antibody-Dependent Cell Cytotoxicity/immunology
MH  - Carcinoma, Small Cell/genetics/immunology/*therapy
MH  - Chemokine CCL2/*genetics
MH  - Dose-Response Relationship, Drug
MH  - *Drug Resistance, Multiple
MH  - Humans
MH  - Killer Cells, Natural/immunology
MH  - Lung Neoplasms/genetics/immunology/*therapy
MH  - Mice
MH  - Mice, Nude
MH  - Neoplasm Transplantation
MH  - RNA, Messenger/metabolism
MH  - Time Factors
MH  - *Transfection
MH  - Tumor Cells, Cultured
EDAT- 1997/04/10 00:00
MHDA- 2000/06/20 09:00
CRDT- 1997/04/10 00:00
PHST- 1997/04/10 00:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1997/04/10 00:00 [entrez]
AID - 10.1002/(SICI)1097-0215(19970410)71:2<170::AID-IJC8>3.0.CO;2-Y [pii]
AID - 10.1002/(sici)1097-0215(19970410)71:2<170::aid-ijc8>3.0.co;2-y [doi]
PST - ppublish
SO  - Int J Cancer. 1997 Apr 10;71(2):170-7. doi: 
      10.1002/(sici)1097-0215(19970410)71:2<170::aid-ijc8>3.0.co;2-y.