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Expression and clinical significance of microRNA-326 in human glioma miR-326 expression in glioma.
MedLine Citation:
PMID:  23292865     Owner:  NLM     Status:  In-Data-Review    
As a suppressor of Hedgehog signaling pathway, microRNA-326 (miR-326) has been demonstrated to control the development of cerebellar neuronal progenitor and tumor cells. More recently, it has been reported that miR-326 was down-regulated in glioblastoma tissues and might regulate the metabolic activity of glioma and glioma stem cells, suggesting the involvement of miR-326 in tumorigenesis and progression of gliomas. However, the role of miR-326 in human glioma has not been clearly understood. Therefore, the aim of this study was to investigate the clinical significance of miR-326 expression in human glioma. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis was used to characterize the expression patterns of miR-326 in 108 glioma and 20 normal brain tissues. The associations of miR-326 expression with clinicopathological factors and prognosis of glioma patients were also statistically analyzed. The expression levels of miR-326 in glioma tissues were significantly lower than those in normal brain tissues (P < 0.001). Additionally, the decreased miR-326 expression in glioma was significantly associated with advanced pathological grade (P = 0.01) and low Karnofsky performance score (KPS, P = 0.03). Moreover, Kaplan-Meier survival and Cox regression analyses showed that low expression of miR-326 (P = 0.01) and advanced pathological grade (P = 0.02) were independent factors predicting poor prognosis for gliomas. Furthermore, subgroup analyses showed that miR-326 expression was significantly associated with poor overall survival in glioma patients with high pathological grades (for grade III-IV: P < 0.001). Down-regulation of miR-326 may have potential value for predicting clinical outcomes in glioma patients with high pathological grades, suggesting that miR-326 is an important candidate tumor suppressor, and its down-regulated expression may contribute to glioma progression.
Shuai Wang; Shengkui Lu; Shaomei Geng; Shucheng Ma; Zhaohui Liang; Baohua Jiao
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Publication Detail:
Type:  Journal Article     Date:  2013-01-06
Journal Detail:
Title:  Medical oncology (Northwood, London, England)     Volume:  30     ISSN:  1559-131X     ISO Abbreviation:  Med. Oncol.     Publication Date:  2013 Mar 
Date Detail:
Created Date:  2013-01-07     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9435512     Medline TA:  Med Oncol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  373     Citation Subset:  IM    
Department of Neurosurgery, Second Hospital of Hebei Medical University, No. 215, Hepingxi Road, Shijiazhuang City, 050000, Hebei Province, China.
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