Abstract
Abstract Ciglitazone is a kind of thiazolidinedione and a potent, selective peroxisome proliferator-activated receptor γ (PPAR γ) ligand and it is active in vivo as an anti-hyperglycemic agent in the murine model. Glucose metabolism plays a key role in the maintenance of energy homeostasis in organisms and changes in cellular glucose uptake rate are found in malignant diseases. Significant increase in glucose consumption can be found in many malignant conditions and research so far has focused on its apoptotic and inhibition of proliferation properties but their role in cell death is unclear. We show that ciglitazone inhibits glucose uptake in ovarian cancer cell through GLUT-1 expression. In this study, we investigated the effect of ciglitazone to GLUT-1 expression and cell proliferation. We further demonstrate that ciglitazone pretreated tumor cell was increased apoptosis dose dependent manner and siGLUT-1 treated tumor cell showed increased apoptosis. Interestingly, not only cancer cell line but also in vivo state, ciglitazone could decrease tumor mass. Specificity protein (Sp) is highly expressed in tissues of prostate cancer, breast carcinomas and lung cancer when compared to normal tissues or cells. Previous studies showed that Sp1 plays an important role in carcinogenesis and metastasis of several human tumor types by regulating growth-related signal transduction, cell cycle control molecules, apoptosis, oncogenes, tumor suppressor genes. In this study there was no relation with apoptosis and SP1 expression. We demonstreated that ciglitazone inhibit glucose uptake in ovarian cancer cell lines and the relationship between ciglitazone and GLUT-1 in ciglitazone induced cell death. Citation Format: Jin Young Kim, So Jin Shin, Keon Uk Park, Young June Jeon, Chi Heum Cho, Eunyoung Ha. Ciglitazone increases ovarian cancer cell death by inhibiting GLUT-1 expression. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1865. doi:10.1158/1538-7445.AM2013-1865
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