Reduced expression of microRNA-497 is associated with greater angiogenesis and poor prognosis in human gliomas
MicroRNA (miR)-497 plays a tumor-suppressive role in several malignancies and is involved in glioma invasiveness and resistance to chemotherapy. To add to the knowledge of the clinical significance of miR-497 in human gliomas, quantitative real-time polymerase chain reaction (qRT-PCR) was performed...
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Veröffentlicht in: | Human pathology 2016-12, Vol.58, p.47-53 |
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Zusammenfassung: | MicroRNA (miR)-497 plays a tumor-suppressive role in several malignancies and is involved in glioma invasiveness and resistance to chemotherapy. To add to the knowledge of the clinical significance of miR-497 in human gliomas, quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression of miR-497 in 110 pairs of freshly prepared glioma and nonneoplastic brain tissues. Then the associations of miR-497 expression with various clinicopathologic characteristics and overall survival of glioma patients were estimated statistically. Gain-of-function assays also were performed to examine the role of miR-497 in glioma angiogenesis. The expression of miR-497 in human glioma tissues was significantly lower than in nonneoplastic brain tissues (P < .001). In addition, low miR-497 expression was significantly associated with advanced World Health Organization grade (P < .001) and low Karnofsky performance scores (P = .02). Moreover, the survival of glioma patients with low miR-497 expression was dramatically shorter than that of patients with high miR-497 expression (P = .001). Forced expression of miR-497 in glioma cells inhibited tube formation by co-cultured human brain microvascular endothelial cells. We also found that miR-497 overexpression in glioma cells led to decreased expression of vascular endothelial growth factor (VEGF). In conclusion, miR-497 may be a favorable prognostic marker in human gliomas, in part by being a negative regulator of angiogenesis, implying its potential as a therapeutic target for this cancer. |
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ISSN: | 0046-8177 1532-8392 |
DOI: | 10.1016/j.humpath.2016.04.022 |