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J. Biol. Chem., Vol. 275, Issue 22, 16618-16625, June 2, 2000
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From the In most cells, transferrin receptor
(TfR1)-mediated endocytosis is a major pathway for cellular iron
uptake. We recently cloned the human transferrin receptor 2 (TfR2)
gene, which encodes a second receptor for transferrin (Kawabata, H.,
Yang, R., Hirama, T., Vuong, P. T., Kawano, S., Gombart, A. F., and
Koeffler, H. P. (1999) J. Biol. Chem. 274, 20826-20832).
In the present study, the regulation of TfR2 expression and function
was investigated. A select Chinese hamster ovary (CHO)-TRVb cell line
that does not express either TfR1 or TfR2 was stably transfected with
either TfR1 or TfR2-
Transferrin Receptor 2-
Supports Cell Growth Both in
Iron-chelated Cultured Cells and in Vivo*
§,,,
, and**
Cedars-Sinai Medical Center, Department of
Medicine, Division of Hematology/Oncology, Burns and Allen Research
Institute, UCLA School of Medicine, Los Angeles, California 90048, the
¶ Department of Hematology, Showa University School of Medicine,
Tokyo 142-8555, Japan, and the Department of Pathology, Center
for the Health Science, UCLA School of Medicine,
Los Angeles, California 90095
cDNA.
TfR2--expressing cells had considerably lower affinity for
holotransferrin when compared with TfR1-expressing CHO cells.
Interestingly, in contrast to TfR1, expression of
TfR2 mRNA in K562 cells was not up-regulated by
desferrioxamine (DFO), a cell membrane-permeable iron chelator. In MG63
cells, expression of TfR2 mRNA was regulated in the
cell cycle with the highest expression in late G1 phase and
no expression in G0/G1. DFO reduced cell
proliferation and DNA synthesis of CHO-TRVb control cells, whereas it
had little effect on TfR2--expressing CHO cells when measured by
clonogenic and cell cycle analysis. In addition, CHO cells that express
TfR2- developed into tumors in nude mice whereas CHO control cells
did not. In conclusion, TfR2 expression may be regulated by the cell
cycle rather than cellular iron status and may support cell growth both
in vitro and in vivo.
*
This work was supported in part by grants from the National
Institutes of Health, United States Department of Defense, California Tobacco Grant, C. and H. Koeffler Fund, Parker Hughes Trust, and an Eli
Lilly International Fellowship (to H. K.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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