H. Serve et al., INHIBITION OF PROLIFERATION AND CLONAL GROWTH OF HUMAN BREAST-CANCER CELLS BY INTERLEUKIN-13, Cancer research, 56(15), 1996, pp. 3583-3588
We tested the influence of recombinant human interleukin (rhIL)-13 and
rhIL-4 on clonal growth of human breast cancer cell lines. rhIL-13 an
d rhIL-4 inhibited clonal growth of three of nine lines to approximate
ly 50% of controls (ED(50), 0.5 ng/ml). rhIL-13 reduced [H-3]thymidine
incorporation in all three cell lines: two showing a minor (84% and 8
3% of controls) and one showing a major response (25% of control). Bot
h cytokines markedly reduced serum-induced G(0/1) exit (approximately
25% versus 60%). I-125-labeled interleukin (IL) 13 binding assays reve
aled high-affinity binding sites for IL-13 on two of the three respond
ing cell lines (K-D approximately 60 pM). (Y124D)IL-4 effectively anta
gonized all effects of rhIL-13 and rhIL-4 arguing for shared receptor
components between them. However, neither rhIL-4 nor (Y124D)IL-4 could
displace I-125-labeled IL-13 from binding, although unlabeled rhIL-13
effectively did so. Using reverse transcription-PCR, we studied the e
xpression of the common gamma chain (gamma(c)) in responding cell line
s, putatively being shared between IL-4 receptor and IL-13 receptor; n
one of the three cell lines express gamma(c). In conclusion, we demons
trate antiproliferative effects of IL-4 and IL-13 on carcinoma cells w
hich express IL-13 binding sites without participation of gamma(c).