INHIBITION OF PROLIFERATION AND CLONAL GROWTH OF HUMAN BREAST-CANCER CELLS BY INTERLEUKIN-13

Citation
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
Citations number
36
Categorie Soggetti
Oncology
Journal title
ISSN journal
00085472
Volume
56
Issue
15
Year of publication
1996
Pages
3583 - 3588
Database
ISI
SICI code
0008-5472(1996)56:15<3583:IOPACG>2.0.ZU;2-T
Abstract
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).