Gene
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Long noncoding RNAs (lncRNAs) have been shown to play an important role in tumor biogenesis and prognosis. The glioma is a grade classified cancer, however, we still lack the knowledge on their function during glioma progression. While previous studies have shown how lncRNAs regulate protein-coding gene epigenetically, it is still unclear how lncRNAs are regulated epigenetically. ⋯ Thirdly, we developed a DESeq2-GSEA-ceRNA-survival analysis strategy to investigate their functions. Particularly, MIR4435-2HG is highly expressed in high-grade glioma and may have an impact on EMT and TNFα signaling pathway by functioning as a miRNA sponge of miR-125a-5p and miR-125b-5p to increase the expression of CD44. Our results revealed the dynamic expression of lncRNAs in glioma progression and their epigenetic regulation mechanism.
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Machine learning (ML) is a powerful technique to tackle many problems in data mining and predictive analytics. We believe that ML will be of considerable potentials in the field of bioinformatics since the high-throughput technology is producing ever increasing biological data. In this review, we summarized major ML algorithms and conditions that must be paid attention to when applying these algorithms to genomic problems in details and we provided a list of examples from different perspectives and data analysis challenges at present.
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Long non-coding RNAs (lncRNA) and circular RNAs (circRNA) that sponge miRNAs could indirectly regulate gene expression, contributing to certain biological processes. This study aimed to investigate the role of non-coding RNAs in the pathogenesis of myocardial ischemia reperfusion-injury (MIRI). MIRI in male C57B/6J mice was induced by left anterior descending coronary artery ligation occlusion for 30 min, and 4 h of reperfusion. ⋯ The lncRNA co-expression network and ceRNA network base on genes in AMPK signaling pathway were then constructed, revealing that ENSMUST00000147762.7 and TUCP_000184 might be key regulators in MIRI induced AMPK activation. The expression levels of AMPK signaling-related RNAs and those involved in the ceRNA network were validated using qRT-PCR. Overall, this study identified potential new targets on AMPK signaling in MIRI.
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Clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 system has ushered in a new era of gene therapy. In this study, we aimed to demonstrate precise CRISPR/Cas9-mediated genome editing of the splicing mutation c.919-2A > G in intron 7 of the SLC26A4 gene, which is the second most common causative gene of congenital hearing loss. We designed candidate single-guide RNAs (sgRNAs) aimed to direct the targeting of Staphylococcus aureus Cas9 to either exon 7 or exon 8 of SLC26A4. ⋯ We subsequently evaluated genome editing in the presence of artificial donor templates to induce precise target modification via homology-directed repair. Using this approach, two different donor plasmids successfully introduced silent mutations within the c.919-2A region of Slc26a4 without evident off-target activities. Overall, these results indicate that CRISPR/Cas9-mediated correction of mutations in the Slc26a4 gene is a feasible therapeutic option for restoration of hearing loss.
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We analysed multiple microarray datasets in the Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) DataSets for messenger RNAs (mRNAs) whose expression is apparently increased in human cholangiocarcinoma (CCA) samples, compared with that in the adjacent normal biliary epithelial tissue. The results revealed that the expression of tripartite motif-containing 59 (TRIM59) was significantly increased in the CCA tissue samples. TRIM59 is a member of the tripartite motif (TRIM) protein family, which contains a highly conserved N-terminal-an interesting new gene (RING) domain regulating transcriptional factors and tumorigenesis. In the present study, we investigated the effects of TRIM59 expression on tumour growth in CCA. ⋯ Our study revealed that TRIM59 is up-regulated in CCA tissues and cell lines and promoted CCA cell proliferation, possibly by affecting the PI3K/AKT/mTOR signalling pathway.