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Blood, Vol. 96 No. 2 (July 15), 2000:
pp. 691-698
Gi and Gq/11 proteins are involved in dissemination of myeloid
leukemia cells to the liver and spleen, whereas bone marrow
colonization involves Gq/11 but not Gi
Ron D. M. Soede,
Yvonne M. Wijnands,
Marga Kamp,
Martin A. van der Valk, and
Ed Roos
From the Divisions of Cell Biology and Molecular Genetics, The
Netherlands Cancer Institute, Amsterdam, The Netherlands.
The migration of leukocytes into tissues is regulated by
chemokines and other chemotactic factors that act on receptors that signal through Gi proteins. It seems likely that the colonization of
tissues during dissemination of hematopoietic tumor cells is similarly
regulated. In fact, dissemination of a T-cell hybridoma, a model for T
lymphoma, was blocked when Gi proteins were inactivated by the S1
catalytic subunit of pertussis toxin that had been transfected into
those cells. Pertussis toxin S1 blocked dissemination of MDAY-D2 murine myeloid leukemia cells to the liver and
spleen, as in T-cell hybridoma cells, but it did not prevent bone
marrow colonization. In contrast, overexpression of a
function-defective mutant of the Gq/11 protein blocked dissemination to
the bone marrow and also prevented Gq/11 dissemination to the liver and spleen. This indicates that the influx of these myeloid cells into all
tissues requires the Gq/11 protein in addition to the Gi protein in the
liver and spleen.
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