Abstract 831: uPAR Expression is Up-regulated in Cervical Cancer

Abstract

Abstract Hypoxia occurs during development of cervical cancer and is considered to correlate with its invasion. Hypoxia induces cancer cells to have more invasive property through the urokinase plasminogen activator receptor (uPAR) expression. Also, poor prognosis of uterine cervical cancer is correlated with hypoxic condition. Thus, we examined the relationship among the uPAR mRNA level and clinical prognostic factors, such as clinical and pathological stage, hemoglobin level, histologic type, tumor marker level and the effect on clinical outcome, using 66 cases of cervical cancer and 10 normal cervical tissues. These factors were evaluated by t test and Spearman's rank correlation coefficient. Survival analysis was performed using Kaplan-Meier curves. The uPAR mRNA level is significantly up-regulated in cervical cancers, compared with that in normal cervixes. The level of hemoglobin was significantly correlated with uPAR mRNA expression. Whereas, no other clinical prognostic factor had correlation with uPAR mRNA expression. Also, the uPAR mRNA level was not correlated with survival. According to the invasion assays, cervical cancer cell lines, CA and CaSki, under hypoxic condition (1% O2) showed more invasive property than those under normoxia. Hypoxia enhanced the endogenous uPAR mRNA level and protein expression by realtime RT-PCR and western blot analysis, respectively. Although we hypothesized that uPAR expression was correlated with tumor invasion and poor prognosis, the results revealed that uPAR mRNA expression was not correlated with survival nor most clinical factors except for the hemoglobin level. Although uPAR seems to be critical for the invasiveness in cervical cancer cell lines, uPAR may not be involved in cervical cancer invasion in vivo. Only real hypoxia may regulate the uPAR mRNA expression in cervical cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 831.