Expression changes for long non-coding RNAs (lncRNAs) have been identified in adult glioblastoma multiforme (GBM) and in a mixture of adult and pediatric astrocytoma. Since adult and pediatric astrocytomas are molecularly different, the mixture of both could mask specific features in each. We determined the global expression patterns of lncRNAs and messenger RNA (mRNAs) in pediatric astrocytoma of different histological grades. Transcript expression changes were determined with an HTA 2.0 array. lncRNA interactions with microRNAs and mRNAs were predicted by using an algorithm and the LncTar tool, respectively. Interactomes were constructed with the HIPPIE database and visualized with the Cytoscape platform. The array showed expression changes in 156 and 207 lncRNAs in tumors (versus the control) and in pediatric GBM (versus low-grade astrocytoma), respectively. Predictions identified lncRNAs that have putative microRNA binding sites, which might suggest that they function as sponges in these tumors. Also, lncRNAs were shown to interact with many mRNAs, such as Pleckstrin homology-like domain, family A, member 1 (PHLDA1) and sulfatase 2 (SULF2). For example, qPCR found long intergenic non-coding RNA regulator of reprogramming (linc-RoR) expression levels upregulated in pediatric GBM when they were compared with control tissues or with low-grade tumors. Meanwhile, PHLDA1 and ELAV-like RNA binding protein 1 (ELAV1) showed expression changes in tumors relative to the control. Our data showed many lncRNAs with expression changes in pediatric astrocytoma, which might be involved in the regulation of different signaling pathways.
Background. Y-RNAs are small noncoding RNAs firstly identified in patients suffering the Sjögren’s syndrome and lupus erythematosus, having different predicted cellular functions. In this work, circulating Y-RNAs were detected in blood serum from pediatric patients with pilocytic or diffuse astrocytoma, by means of the HTA 2.0 arrays. In addition, a bioinformatic approximation of the possible biological functions of Y-RNAs was determined with the “Random Forest” and “Vector Support Machine” algorithms. Results. Data showed a differential expression of RNY-3, RNY-4, and -5 in tumors relative to the control. Meanwhile, RNY-1 was shown to be highly upregulated in the Diffuse condition versus the Pilocytic one. The bioinformatic analysis showed the interaction of all these Y-RNAs with different proteins, but RNY-4 and RNY-5 had the highest scores of interaction with the Claudin domain-containing protein 1, isoform α and Toll-like receptor 5, and the Hyaluronidase-1 isoform 3. Because Y-RNAs are processed in vivo to produce fragments through RNase processing, a second analysis was performed to determine the Y-RNAs loop domain interactions with these receptors. Results showed the highest score of interaction for RNY-3/B cell receptor CD22 isoform 1, followed by RNY-4/Toll-like receptor 7 and 3. Conclusions. Altogether, our results showed, for the first time a differential expression of circulating Y-RNAs in pediatric astrocytoma, allowing to distinguish pediatric patients without cancer from patients with pediatric diffuse or pilocytic astrocytoma and their potential involvement in regulating diverse biological processes, such as immune activation or suppression, cell signaling, selective transcription, and cell proliferation through DNA replication activation.
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