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Effect of glucocorticoids on the biologic activities of myeloma cells:
inhibition of interleukin-1 beta osteoclast activating factor-induced bone
resorption
H Ishikawa, H Tanaka, K Iwato, O Tanabe, H Asaoku, M Nobuyoshi, I Yamamoto, M Kawano and A Kuramoto
Department of Internal Medicine, Hiroshima University, Japan.
Regulatory effects of glucocorticoids (dexamethasone) on myeloma cells as
well as bone resorption in multiple myeloma were investigated.
Glucocorticoids significantly inhibited proliferation of myeloma cells, and
decreased the messenger RNA (mRNA) expressions of interleukin-6 (IL- 6) and
secretory type immunoglobulin G (IgG). The inhibitory effects of
glucocorticoids on myeloma cell proliferation could be due to the decreased
expression of IL-6 mRNA, decreased IL-6 production, and thus suppression of
autocrine growth by IL-6, which is an autocrine growth factor for myeloma
cells as reported previously (Nature 332:83, 1988). Glucocorticoids also
inhibited M-protein secretion by decreasing the levels of secretory type Ig
mRNA. On the other hand, because IL-1 beta rather than lymphotoxin is
considered to be a major osteoclast activating factor (OAF) produced by
myeloma cells, and glucocorticoids decreased the expression of IL-1 beta
mRNA and markedly suppressed the bone resorbing activity induced by IL-1
beta OAF in 45Ca-release bone resorption assay, it is suggestive that
glucocorticoids could inhibit bone resorption induced by IL-1 beta OAF in
multiple myeloma. Therefore, from these data it is concluded that
glucocorticoids could be more effective chemotherapeutic agents in multiple
myeloma than we expected, especially with regards to the inhibitory effects
on proliferation and M-protein secretion from myeloma cells, as well as
bone resorption by myeloma cells.
Volume 75,
Issue 3,
pp. 715-720,
02/01/1990
Copyright © 1990 by The American Society of Hematology
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