Interleukin-6 inhibits the potent stimulatory action of androgens, glucocorticoids and interleukin-1α on apolipoprotein D and GCDFP-15 expression in human breast cancer cells

✍ Scribed by Yves Blais; Keiko Sugimoto; Marie-Claude Carrière; Darrow E. Haagensen; Fernand Labrie; Jacques Simard

• Publisher: John Wiley and Sons
• Year: 1995
• Tongue: French
• Weight: 670 KB
• Volume: 62
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.2910620614

✦ Synopsis

Our study was designed to investigate the potential interaction between steroid hormones and interleukin-6 (IL-6) in the regulation of apolipoprotein D (apo-D) and gross cystic disease fluid protein I 5 (GCDFP-15) expression in ZR-75-I human breast cancer cells. We first observed that exposure to IL-6 for 6-1 4 days decreased basal apo-D and GCDFP-I 5 secretion by 50% and 23%, respectively. In the same experiment, such treatment with IL-6 decreased cell proliferation by approximately 40% after 6 and 14 days of incubation. Exposure to IL-6 markedly decreased di hydrotestosterone (DHT)-induced apo-D and GCDFP-15 release, with a half-maximal effect measured at 13 U/ml. A similar inhibitory action of IL-6 was observed on the glucocorticoid dexamethasone (DEX)-induced apo-D and GC-DFP-I 5 secretion. The sensitivity of the apo-D and GCDFP-I 5 response to the stimulatory action of DHT or DEX was, however, not changed by concomitant exposure to IL-6. The inhibitory effect of IL-6 on the secretion of these two biochemical markers was additive to that of 17P-estradiol. In addition, IL-6 blocked the stimulatory effect of interleukin-la (ILla) on apo-D and GCDFP-I 5 secretion. Our results show that IL-6 is a potent inhibitor of basal as well as androgen-, glucocorticoidand IL-I a-induced apo-D and GCDFP-I 5 secretion in ZR-75-I human breast cancer cells, while cell proliferation is inhibited by this cytokine.