Abstract
Abstract Glioblastoma multiforme (GBM) is highly invasive and resistant to current therapies. The aggressiveness of brain tumor is attributed to GBM stem cells (GSC) that release inflammatory cytokines, and exacerbate inflammation in tumor microenvironment, critically affecting GBM survival and invasiveness. The glycoprotein pentraxin-3 (PTX3), a modulator of tumor-associated inflammation, is known to be correlated with tumor grade and severity of malignancies of some cancers. However, little is known about the role of PTX3 in GBM growth and invasion. In this study, we examined the role of PTX3 in GSCs exhibiting various degree of invasiveness. From patient brain tumors, our team has isolated the small subsets of glioblastoma stem cells (GSCs) and are validated for their self-renewal and multi-lineage potential. Our studies have shown that these GSCs efficiently form orthotopic brain tumors in immune-deficient mice. Our results show that conditioned media from GSCs promote pro-angiogenic tube formation from endothelial cells. GSCs that are grown in the absence of growth factors EGF and bFGF, formed efficient xenografts in immune-deficient mice and showed increased dispersal in the mice brain. Interestingly, polymerase chain reaction (RT-PCR) and immunofluorescence staining showed upregulated expression of PTX3 in these GSCs, and correlated with the degree of invasiveness. Differentiation of GSC into astrocytes in vitro, lead to decreased expression of PTX3. In support of this, recent histochemical study has shown that PTX3 levels correlate with GBM grade and is a candidate biomarker for cancer progression. Thus, PTX3 may represent a new target and marker of inflammation for glioma malignancy. Citation Format: Umadevi V. Wesley, Paul Clark, John S. Kuo, Robert J. Dempsey. Dysregulated expression of pentraxin-3 in glioblastoma (GBM) stem cells: Implications for GBM invasion and progression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4773. doi:10.1158/1538-7445.AM2017-4773
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