Abstract
Abstract Steroid sulfatase (STS) is responsible for the conversion of estrone sulfate to estrone that can stimulate growth in endocrine-dependent tumors such as breast and prostate cancer. Although STS is considered as a therapeutic target for the estrogen-dependent diseases, cellular function of STS are still not clear. Previously, we found that tumor necrosis factor (TNF)-α significantly enhances steroid sulfatase expression in PC-3 human prostate cancer cells through PI3K/Akt-dependent pathways. Here, we studied whether bacterial lipopolysaccharides (LPS) which are known to induce TNF-α may increase STS expression. Treatment with LPS in PC-3 cells induces STS mRNA and protein in concentration- and time-dependent manners. Because LPS-induced STS mRNA expression was strongly suppressed by NF-κB inhibitors such as Bay 11-7082 and bortezomib, the involvement of NF-κB pathways on STS expression was suggested. To determine whether IkBα is involved in NF-κB-dependent STS expression, the effect of IKKα siRNA was elucidated. IKKα siRNA significantly suppressed STS mRNA and protein expression. Interestingly, overexpression of STS by transfecting expression vector induced wound healing effect whereas knockdown of STS by siRNA significantly decreased wound healing effect in PC-3 cells. Moreover, treatment with LPS in STS knockdowned cells recovered wound healing effect. Taken together, these results strongly suggest that STS may contribute tumor cell migration. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4122. doi:1538-7445.AM2012-4122
Published Version
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