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Journal of Biomedicine and Biotechnology
Volume 2012, Article ID 970761, 6 pages
Research Article

Increased Expression of microRNA-17 Predicts Poor Prognosis in Human Glioma

Department of Neurosurgery, Second Hospital of Hebei Medical University, No. 215 Hepingxi Road, Hebei Province, Shijiazhuang City 050000, China

Received 30 September 2012; Accepted 22 October 2012

Academic Editor: Thomas Liehr

Copyright © 2012 Shengkui Lu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Aim. To investigate the clinical significance of microRNA-17 (miR-17) expression in human gliomas. Methods. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis was used to characterize the expression patterns of miR-17 in 108 glioma and 20 normal brain tissues. The associations of miR-17 expression with clinicopathological factors and prognosis of glioma patients were also statistically analyzed. Results. Compared with normal brain tissues, miR-17 expression was significantly higher in glioma tissues ( ). In addition, the increased expression of miR-17 in glioma was significantly associated with advanced pathological grade ( ) and low Karnofsky performance score (KPS, ). Moreover, Kaplan-Meier survival and Cox regression analyses showed that miR-17 overexpression ( ) and advanced pathological grade ( ) were independent factors predicting poor prognosis for gliomas. Furthermore, subgroup analyses showed that miR-17 expression was significantly associated with poor overall survival in glioma patients with high pathological grades (for grade III~IV: ). Conclusions. Our data offer the convinced evidence that the increased expression of miR-17 may have potential value for predicting poor prognosis in glioma patients with high pathological grades, indicating that miR-17 may contribute to glioma progression and be a candidate therapeutic target for this disease.