The resistance of macrophage-like tumour cell lines to growth inhibition by lipopolysaccharide and pertussis toxin

Xie, Yue, von Gavel, Stephanie, Cassady, A. Ian, Stacey, Katryn J., Dunn, Timothy L. and Hume, David A. (1993) The resistance of macrophage-like tumour cell lines to growth inhibition by lipopolysaccharide and pertussis toxin. British Journal of Haematology, 84 3: 392-401. doi:10.1111/j.1365-2141.1993.tb03092.x


Author Xie, Yue
von Gavel, Stephanie
Cassady, A. Ian
Stacey, Katryn J.
Dunn, Timothy L.
Hume, David A.
Title The resistance of macrophage-like tumour cell lines to growth inhibition by lipopolysaccharide and pertussis toxin
Journal name British Journal of Haematology   Check publisher's open access policy
ISSN 0007-1048
1365-2141
Publication date 1993
Year available 1993
Sub-type Article (original research)
DOI 10.1111/j.1365-2141.1993.tb03092.x
Volume 84
Issue 3
Start page 392
End page 401
Total pages 10
Place of publication Chichester, West Sussex, United Kingdom
Publisher Wiley-Blackwell Publishing Ltd
Collection year 1994
Language eng
Formatted abstract
The process of tumorigenesis is frequently associated with resistance to growth inhibition by physiological regulators of normal cells. Murine macrophage-like cell lines BAC1.2F5, RAW264, J774.1A and PU5/1.8 were resistant to growth inhibition by bacterial lipopolysaccharide (LPS) and pertussis toxin, agents that blocked growth of primary bone marrow-derived macrophages (BMDM) in the presence of macrophage colony-stimulating factor (CSF-1). The resistance of the CSF-1-dependent cell line BAC1.2F5 to growth inhibition by pertussis toxin argues against the possibility that pertussis toxin-sensitive G proteins are essential for the pathway of growth stimulation by CSF-1. Conversely, these data add further weight to the argument that LPS mediates some of its biological activities by mimicking the action of pertussis toxin and inhibiting G protein function. The resistance of cell lines to LPS and pertussis toxin was not correlated with any alteration in the expression of mRNA encoding any of three pertussis-toxin sensitive G protein α subunits. The pattern of G protein expression was consistent between primary cells and tumour cells, suggesting that this is a differentiation marker. In particular, G(i)α2 mRNA was expressed at remarkably high levels in all of the cells. The specificity of LPS resistance was investigated by studying down-regulation of CSF-1 binding and induction of protooncogene c-fos and tumour necrosis factor (TNF) mRNA. BAC1.2F5 cells were LPS-resistant in each of these assays. In CSF-1 binding, RAW264 and J774.1A responded in the same way as bone marrow-derived macrophages but required higher doses of LPS, whereas c-fos and TNF mRNA were induced in these cells at concentrations that did not inhibit growth. In PU5/1.8 cells, CSF-1 binding was already very low and was not further down-regulated, but c-fos and TNF mRNA was inducible by LPS. By contrast to primary macrophages, the cell lines did not respond to LPS with down-regulation of c-fms mRNA, which encodes the CSF-1 receptor. Hence, the resistance of macrophage-like tumour cells to LPS and pertussis toxin was specific to the pathways controlling growth, and was correlated with altered regulation of the CSF-1 receptor
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Chemistry and Molecular Biosciences
 
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Created: Fri, 06 Sep 2013, 17:32:04 EST by Dr Katryn Stacey on behalf of School of Chemistry & Molecular Biosciences