A possible explanation for why the two signatures did not agree e

A possible explanation for why the two signatures did not agree exactly may be because of differences in the target population and/or the entry criteria. In another study, a 5-miRNA signature was identified as a prognostic biomarker in Chinese patients with primary GBM [1]. This 5-miRNA selleck products signature (miR-181d, miR-518b, miR-524-5p, miR-566, and miR-1227) was significantly associated with improved overall survival for GBM patients.

Interestingly, none of the five miRNAs in this signature overlapped with the miRNAs in our 23-miRNA signature, probably because different patient populations and datasets were used in the two studies. We further investigated the six miRNAs that were common to

the 10-miRNA and 23-miRNA signatures. selleck chemicals llc Some studies have shown that miR-183 was significantly down-regulated in osteosarcoma and may subsequently promote migration, invasion, and recurrence of osteosarcoma [16]. In our study, we found that miR-183 was a favorable predictor for GBM, which was consistent with its effect in osteosarcoma. In advanced colorectal cancer, miR-148a expression was the most significantly downregulated, which resulted in a worse therapeutic response and poor overall survival [17]. A similar effect was found in GBM, and, in our study, miR-148a was classified as one of the risky biomarkers for GBM. In a study of adult T-cell leukemia, miR-155 was identified as a novel unfavorable biomarker for disease progression and prognosis [18]. Another study reported that elevation of plasma miR-155 was associated with shorter survival times in non-small cell lung cancer [19]. These findings were consistent with our results for the function of miR-155. MiR-221 and its paralogue miR-222 are known

inhibitors of angiogenesis, which act by blocking cell migration and proliferation in endothelial cells [20, 21]. Other studies have reported different functions for miR-221, suggesting that miR-221 was also associated with induction of angiogenesis [22, 23]. In our research, miR-221 and miR-222 were identified as unfavorable indictors for GBM. In a study into chronic lymphocytic leukemia, miR-34a and miR-17-5p were found to be downregulated in Thiamine-diphosphate kinase chronic lymphocytic leukemia patients with tumor protein p53 (TP53) abnormalities, indicating that higher expression levels of miR-34a and miR-17-5p may predict a better clinical selleckchem outcome for these patients [24]. In TCGA, the IDH1 mutation-type samples account for only 10–16% of the GBMs, most of which are secondary GBMs. Our results provided a robust clinical prognostic indicator for GBM patients with wild-type IDH1. However, we still have no idea how exactly this 23-miRNA signature worked in GBM. Clearly, the mechanisms behind the roles of these miRNAs require further investigation.

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