Abstract

Abstract Glioblastomas are characterized by aggressive invasion into normal brain tissues, thus limiting complete removal by surgical resection resulting in recurrence. Our identified molecule involved in glioma invasion is important for developing targeted effective therapies in the malignant glioma. Cancer stem cells are capable for self-renewing and are thought to be responsible for tumor metastasis and dissemination. However, the invasive activities of cancer stem cells have not been fully understood. To investigate a role of glioma stem cells in the tumor invasion, tumor sphere culture was established from mouse glioma RSV-M cells. The high tumorigeneity and aggressive migration of RSV-M tumor sphere were observed in intracranial transplantation. Quantitative RT-PCR analysis showed the enhanced expression of metastasis-related genes in RSV-M tumor sphere. Of these, MUC18/MCAM also highly expressed in tumor sphere derived from human glioma cell lines. Importantly, CD133-positive fraction of glioma sphere culture isolated from glioblastoma patients contained a cell population expressing MUC18 but CD133-negative fraction not. To examine a function of MUC18 in glioma cells, the expression or knockdown construct for the gene were introduced into human glioma cells. Over-expression of MUC18 in the glioma cells increased their invasive capacity and clonogenicity in comparison to the parent or knockdown cells. In addition, expression of some metastasis-related genes was up-regulated in MUC18-over-expressing cells. These results suggest that enhanced MUC18 expression of glioma stem cells may contribute to the aggressive invasion of this tumor. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3402. doi:10.1158/1538-7445.AM2011-3402

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.