Watson J M, Berek J S, Martínez-Maza O
Department of Microbiology & Immunology, UCLA School of Medicine.
Gynecol Oncol. 1993 Apr;49(1):8-15. doi: 10.1006/gyno.1993.1077.
In previous work, we saw that interleukin-6 (IL-6), a multifunctional cytokine, is produced by epithelial ovarian cancer cells and that ovarian cancer cells express the IL-6 receptor. Here, we examined the possibility that IL-6 acts as an autocrine growth factor for ovarian cancer cells. Inhibition of IL-6 gene expression by exposure to IL-6 antisense oligonucleotides resulted in greatly decreased cellular proliferation. Exposure of ovarian cancer cell lines (CAOV-3, OVCAR-3, and OC-436), to 1-5 microM of a 15-base single-stranded antisense IL-6 oligodeoxynucleotide, specific for a sequence in the second coding exon of the IL-6 gene, resulted in decreased IL-6 production and a > 80-85% inhibition of cellular proliferation. However, the addition of exogenous IL-6 failed to restore the proliferation of the antisense-treated cells. Antibodies to IL-6 did not consistently inhibit cell growth nor did rIL-6 enhance precursor frequency in a limiting dilution analysis. These results suggest that IL-6 does not directly induce the proliferation of ovarian cancer cells although endogenous IL-6 production is needed for optimal cell growth. As the majority of epithelial ovarian cancers produce IL-6, the direct specific inhibition of IL-6 gene expression is of potential therapeutic value.
在先前的研究中,我们发现多功能细胞因子白细胞介素-6(IL-6)由上皮性卵巢癌细胞产生,且卵巢癌细胞表达IL-6受体。在此,我们研究了IL-6作为卵巢癌细胞自分泌生长因子的可能性。通过暴露于IL-6反义寡核苷酸来抑制IL-6基因表达,导致细胞增殖大幅下降。将卵巢癌细胞系(CAOV-3、OVCAR-3和OC-436)暴露于1 - 5 microM的15碱基单链反义IL-6寡脱氧核苷酸(针对IL-6基因第二个编码外显子中的一个序列),导致IL-6产生减少,细胞增殖受到> 80 - 85%的抑制。然而,添加外源性IL-6未能恢复反义处理细胞的增殖。在有限稀释分析中,IL-6抗体并不能持续抑制细胞生长,重组IL-6也不能提高前体细胞频率。这些结果表明,尽管最佳细胞生长需要内源性IL-6的产生,但IL-6并不直接诱导卵巢癌细胞的增殖。由于大多数上皮性卵巢癌产生IL-6,直接特异性抑制IL-6基因表达具有潜在的治疗价值。