Abstract
Abstract The malignant glioma is the most common primary human brain tumor, and its migration and invasiveness away from the primary tumor mass is considered a leading cause of tumor recurrence and treatment failure. Recently, gene expression profiling revealed CD99, which is a transmembrane glycoprotein, is more expressed in malignant glioma than in normal brain. It has been implicated in cell adhesion and migration in various cells, even if the function of this gene is not understood clearly. This gene has two isoforms of wild-type and splicing variant. We revealed that only wild-type CD99 is expressed in human glioma cells and tissues. Through MTS, colony-forming, and anoikis assays, we found that wild-type CD99 in glioma cells has enough resistance for anoikis and ability to survive and grow in anchorage independence, as is opposed to previous reports in other tumors. Using tissue microarray, we validated that CD99 demonstrates higher expression in gliomas compared to non-neoplastic brain. We inhibited CD99 expression by siRNA and demonstrated decreased glioma cell migration and invasion. In contrast, when CD99 was over-expressed in glioma cells, we observed enhancement of cell migration and invasiveness. Orthotopic brain tumor model with nude mice harboring CD99 overexpressing glioma cells results in significant decreased survival rate, compared to control mice. Moreover, higher invasiveness is observed in overexpressing mice by pathological review. Taken together, our findings suggest that CD99 play an important role in the migration and invasion of human gliomas. CD99 could be a target to inhibit migration and invasion especially in CD99-expressing gliomas. 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 2355. doi:10.1158/1538-7445.AM2011-2355
Sign-in/Register to access full text options 
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 callDisclaimer: 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.
