Abstract

Abstract Tumor progression requires tumor angiogenesis, as newly-formed blood vessels supply necessary oxygen and nutrition to the growing tumor. Many unknowns remain in our understanding of the cancer metastasis process. Pentraxin3 (PTX3) is categorized as a long pentraxin in the pentraxin family and is produced by macrophages and vascular endothelial cells. PTX3 concentrations reportedly increase with exposure to IL-1 and TNF-α. Recently, PTX3 has gained attention as a potential marker that reflects inflammation in blood vessels, as well as that which may predict the onset of various diseases, including vascular diseases. The present study examined whether or not an analysis of PTX3 expression may contribute to a mechanistic understanding of carcinogenesis (metastasis) of cervical cancer. Subjects and Methods: Cervical Cancer Cell Lines A comparative study of PTX3 was performed at the protein level and the RNA level by cultivating each of the cervical cancer cell lines CasKi and SiHa under normal conditions and under hypoxic conditions. Clinical Tissue Samples Normal cervical tissues (n=7) and cervical cancer tissues (n=20) were collected from subjects after an explanation of the study was given and consent was obtained. PTX3 expression in both groups was compared. All measurements were taken using ELISA, Western blot, and real time RT-PCR methods. Results: Increased PTX3 expression was observed both at the protein level and at the RNA level in cervical cancer cell lines grown under hypoxic conditions. Conversely, in clinical samples, we observed many samples for which PTX3 expression decreased in cervical cancer samples, contrary to our expectations. Discussion: These results indicate a potential role of PTX3 in the carcinogenesis mechanism of cervical cancer. Further, PTX3 may exhibit cytoprotective effects, which may have played a role in our present study. Future investigation of these results is necessary. 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 3287.

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