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¹ Department of Oncology, National Taiwan University Hospital, No. 7 Chung-Shan South Rd, Taipei 10016, Taiwan
² Department of Internal Medicine, National Taiwan University Hospital, Taiwan
³ Division of Cancer Research, National Health Research Institutes, No. 7 Chung-Shan South Rd, Taipei 10016, Taiwan
⁴ Institute of Toxicology, National Taiwan University College of Medicine, No. 1 Jen Ai Road Section 1, Taipei 100, Taiwan
⁵ Department of Internal Medicine, National Taiwan University College of Medicine, Taiwan
⁶ Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, Taiwan

(Requests for offprints should be addressed to A-L Cheng; Email: Andrew{at}ha.mc.ntu.edu.tw)

Glucocorticoids (GCs) are commonly co-administered with cisplatin in the treatment of patients with carcinomas to prevent drug-induced allergic reaction, nausea and vomiting. Although GC receptor (GR) is ubiquitous in carcinoma cells and has been linked to signal transduction pathways pertinent to cell growth and apoptosis, little is known regarding the possible effect of GC on the chemosensitivity of carcinomas. Our previous study demonstrated that dexamethasone (DEX) enhances the cytotoxicity to cisplatin in a GR-rich human cervical carcinoma cell line, SiHa. In this study, we found that this cisplatin cytotoxicity-enhancing effect of DEX correlated well with its effect on abrogating the cisplatin-induced activation of nuclear factor kappa B (NF-B). RU486, a structural homologue of DEX, partially reversed this cytotoxicity-enhancing effect of DEX, a finding consistent with the well-known partial reversing effect of RU486 on DEX-induced NF-B suppression. Furthermore, expression of a dominant-negative truncated IB gene in SiHa cells completely abolished the cisplatin cytotoxicity-enhancing effect of DEX. Our data suggest that the specific action of DEX on GR may enhance the cytotoxicity of cisplatin in selected GR-rich cancer cells by suppressing NF-B activation.

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