Ovarian cancer is the leading cause of cancerassociated mortality in the female reproductive system. Interleukin (IL)-33 and its receptor IL 1 receptor like 1 (also termed ST2) are expressed by many cell types including epithelial cells. The role of IL-33 in the pathogenesis of neoplasia remains controversial. The authors previously demonstrated that IL-33 inhibits the growth of pancreatic cancer cells. The present study was performed to explore if IL-33 has any direct effects on ovarian cancer cells. A clonogenic survival assay, immunohistochemistry (IHC), proliferation kit and caspase-3 activity kit were all used to evaluate the direct effects of IL-33 on cell proliferation and apoptosis of a widely studied ovarian cancer cell line, A2780. The possible molecular mechanisms were further evaluated with reverse transcription-polymerase chain reaction and IHC. It was demonstrated that the percentage of colonies and the optical density value of cancer cells were all increased in the presence of IL-33; however, the relative caspase-3 activity in cancer cells was decreased in the presence of IL-33. Molecular mechanism studies revealed that the pro-proliferative effect of IL-33 on cancer cells was associated with decreased levels of p27, and the anti-apoptotic effect of IL-33 was associated with levels of Fas cell surface death receptor (Fas) and tumor necrosis factor-related apoptosis-inducing ligand receptor 1 (TRAILR1). Therefore, IL-33 promoted proliferation and inhibited apoptosis of ovarian cancer cells by downregulation of p27, Fas and TRAILR1. Contrary to previous studies demonstrating an anti-tumor effort in pancreatic cancer, the results of the present study indicated that IL-33 exhibited a significant onco-promoting effect on ovarian cancer. Accordingly, the inhibition of IL-33 may be a promising therapeutic strategy for ovarian cancer.
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