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Clear cell renal cell carcinoma (ccRCC) is a malignant tumor originating from the renal tubular epithelium. Although the microRNAs (miRNAs) transcriptome of ccRCC has been extensively studied, the role of miRNAs editing in ccRCC is largely unknown. By analyzing small RNA sequencing profiles of renal tissues of 154 ccRCC patients and 22 normal controls, we identified 1025 miRNA editing sites from 246 pre-miRNAs. There were 122 editing events with significantly different editing levels in ccRCC compared to normal samples, which include two A-to-I editing events in the seed regions of hsa-mir-376a-3p and hsa-mir-376c-3p, respectively, and one C-to-U editing event in the seed region of hsa-mir-29c-3p. After comparing the targets of the original and edited miRNAs, we found that hsa-mir-376a-1_49g, hsa-mir-376c_48g and hsa-mir-29c_59u had many new targets, respectively. Many of these new targets were deregulated in ccRCC, which might be related to the different editing levels of hsa-mir-376a-3p, hsa-mir-376c-3p, hsa-mir-29c-3p in ccRCC compared to normal controls. Our study sheds new light on miRNA editing events and their potential biological functions in ccRCC. [ABSTRACT FROM AUTHOR]

Background. Insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) plays a key role in tumorigenesis and tumor progression. Lung cancer is the leading cause of cancer-related death in men and women all over the world. However, the relationship between IGF2BP3 and small-cell lung cancer (SCLC) has not been reported yet. Methods. SCLC and normal samples (GSE19945 and GSE149507) were obtained in the Gene Expression Omnibus (GEO) dataset. Differential genes were screened by R software, and functional analysis and signal pathway enrichment analysis were carried out. In addition, we used the survival analysis database to analyze the relationship between prognosis and gene expression. Besides, immunohistochemistry (IHC) and quantitative real-time PCR (qPCR) were used for further research. Results. Five differentially expressed miRNAs and 9 differentially expressed mRNAs were selected by using R software. Survival analysis database results show that C7, CLIC5, PRDX1, IGF2BP3, and LDB2 were related the overall survival of patients with SCLC. Furthermore, multivariate analysis included that IGF2BP3 was independent risk factors for SCLC patients. Besides, gene function and signal pathway enrichment analysis showed that differentially expressed miRNAs were involved in the process of tumorigenesis and development. Furthermore, IHC and qPCR outcomes showed that the expression level of hsa-miR-182, hsa-miR-183, and IGF2BP3 was differentially expressed in normal lung tissues (NLTs) and SCLC tissues (SCLCTs). Conclusions. Our results concluded that hsa-miR-182, hsa-miR-183, and IGF2BP3 may take part in the development of SCLC. [ABSTRACT FROM AUTHOR]

Huntington's disease (HD) is a neurodegenerative disease. MicroRNAs (miRNAs) are small non-coding RNAs that mediate post-transcriptional regulation of target genes. Although miRNAs are extensively edited in human brains, the editome of miRNAs in brains of HD patients is largely unknown. By analyzing the small RNA sequencing profiles of brain tissues of 28 HD patients and 83 normal controls, 1182 miRNA editing sites with significant editing levels were identified. In addition to 27 A-to-I editing sites, we identified 3 conserved C-to-U editing sites in miRNAs of HD patients. 30 SNPs in the miRNAs of HD patients were also identified. Furthermore, 129 miRNA editing events demonstrated significantly different editing levels in prefrontal cortex samples of HD patients (HD-PC) when compared to those of healthy controls. We found that hsa-mir-10b-5p was edited to have an additional cytosine at 5'-end in HD-PC, and the edited hsa-mir-10b repressed GTPBP10 that was often downregulated in HD. The down-regulation of GTPBP10 might contribute to the progression of HD by causing gradual loss of function of mitochondrial. These results provide the first endeavor to characterize the miRNA editing events in HD and their potential functions. [ABSTRACT FROM AUTHOR]

• Selecting gold core silver shell nanoparticles as substrates to amplify spectral differences. • Compared with the sandwich sensing mode, the integration of the sensing model based on Raman frequency shift eliminates issues of reproducibility, multiple sampling steps, and long reaction time. • The surface-enhanced Raman scattering analysis platform has satisfactory sensitivity and a detection limit as low as aM level. • This surface-enhanced Raman scattering analysis platform can serve as a potential tool for clinical diagnosis of cervical cancer. Cervical cancer is the most common gynaecological tumor. The development of a sensor for the ultrasensitive detection of cervical cancer is significant in guaranteeing its prognosis. Herein, we proposed a novel surface-enhanced Raman scattering (SERS) analysis platform using a frequency shifts-based sensing model for rapid and ultrasensitive microRNA (miRNA) assay. During the analysis process, miR-21 can be captured by the single-stranded DNA (ssDNA) modified on the platform which is complementary pairing with miR-21. The connection of miR-21 can lead to the variation of the molecular weight and result in the deformation extent of the Raman report molecule 6Thioguanine (6TG); thus, the peak at 1301 cm−1 due to the ring C–N stretches of 6TG shifts to lower frequency. The detection limit (LOD) of the proposed SERS analysis platform is as low as 8.32 aM. Moreover, the platform also has excellent specificity and repeatability, with the relative standard deviation (RSD) value of 6.53 %. Serum samples of cervical cancer patients and healthy subjects were analyzed via the platform and the accuracy of the detection results was verified by qRT-PCR, revealing that SERS results and qRT-PCR results have high homogeneity. Thus, the platform can serve as a potential tool for clinical diagnosis of cervical cancer. [ABSTRACT FROM AUTHOR]

Background. Ewing's sarcoma (ES) is the most common malignant primary bone tumor in children and adolescents. This study is aimed at developing new prognostic markers and building a microRNA-mRNA network in the development of ES. Method. GSE80201 and GSE39262 were downloaded from the Gene Expression Omnibus (GEO) database. Bioinformatics analysis was used to download and process data. The coexpression of differentially expressed microRNAs (DEMs) and genes (DEGs) was selected by using R software. The FunRich database was utilized to perform cellular component (CC), molecular function (MF), and biological process (BP) enrichment analysis. Cytoscape and ClueGO were used to perform Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis and construct the mRNA-microRNA network. The Kaplan-Meier Plotter was used to perform prognosis analysis between the expression level of genes we selected and overall survival (OS) of patients with ES. Univariate analysis and multivariate analysis were carried out to research the prognostic value of identified mRNA expression in ES according to TCGA database. Results. By using bioinformatics analysis, 10 DEMs and 5 target mRNAs were identified. Based on the KmPlot software, COL1A2, COL3A1, and TGFBI were significantly related to the OS of patients with ES. High COL3A1 mRNA expression was correlated with distant metastasis, margin status, and poor overall survival of ES. Besides, multivariate analysis indicated that COL3A1 was an independent risk factor for ES patients. Conclusions. In conclusion, our results suggest that COL3A1 and its related molecules may be a potential diagnostic and prognostic biomarker for patients with ES. [ABSTRACT FROM AUTHOR]

Ovarian cancer is a kind of cancer from the female genital tract; the molecular mechanism still needs to be explored. lncRNA plays a vital role in tumorigenesis and development. Our aim was to identify oncogenic lncRNAs in ovarian cancer and explore the potential molecular mechanism. SNHG15 was initially identified by using GEO datasets (GSE135886 and GSE119054) and validated by tumor tissues and the cell line, identifying that SNHG15 was upregulated in ovarian cancer. Besides, high SNHG15 indicated poor prognosis in ovarian cancer. Furthermore, knockdown SNHG15 suppresses ovarian cancer proliferation and promotes apoptosis. Mechanistically, SNHG15 promotes proliferation through upregulated CDK6 via sponging miR-370-3p. Taken together, our findings emphasize the important role of SNHG15 in ovarian cancer, suggesting that SNHG15 may be a promising target for ovarian cancer. [ABSTRACT FROM AUTHOR]

Background. Osteosarcoma is a malignant bone tumor composed of mesenchymal cells producing osteoid and immature bone. This study is aimed at developing novel potential prognostic biomarkers and constructing a miRNA-mRNA network for progression in osteosarcoma. Method. GSE70367 and GSE70414 were obtained in the Gene Expression Omnibus (GEO) database. GEO software and the GEO2R calculation method were used to analyze two gene profiles. The coexpression of differentially expressed miRNAs (DEMs) and genes (DEGs) was identified and searched for in the FunRich database for pathway and ontology analysis. Cytoscape was utilized to construct the mRNA-miRNA network. Survival analysis of identified miRNAs and mRNAs was performed by utilizing the Kaplan-Meier Plotter. Besides, expression levels of DEMs and target mRNAs were verified by performing quantitative real-time PCR (qRT-PCR) and Western blot (WB). Results. Six differentially expressed microRNAs (DEMs) were identified, and 8 target genes were selected after screening. By using the KM Plotter software, miRNA-124 and ARHGEF3 were obviously associated with the overall survival of patients with osteosarcoma. Furthermore, ARHGEF3 was found downregulated in osteosarcoma cells by performing qRT-PCR and WB experiments. Results also showed that downregulated ARHGEF3 may associate with invasion, metastasis, and proliferation. Conclusions. By using microarray and bioinformatics analysis, DEMs were selected, and a complete miRNA-mRNA network was constructed. ARHGEF3 may act as a therapeutic and prognostic target of osteosarcoma. [ABSTRACT FROM AUTHOR]

Dabrafenib resistance is a significant problem in melanoma, and its underlying molecular mechanism is still unclear. The purpose of this study is to research the molecular mechanism of drug resistance of dabrafenib and to explore the key genes and pathways that mediate drug resistance in melanoma. GSE117666 was downloaded from the Gene Expression Omnibus (GEO) database and 492 melanoma statistics were also downloaded from The Cancer Genome Atlas (TCGA) database. Besides, differentially expressed miRNAs (DEMs) were identified by taking advantage of the R software and GEO2R. The Database for Annotation, Visualization, and Integrated Discovery (DAVID) and FunRich was used to perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis to identify potential pathways and functional annotations linked with melanoma chemoresistance. 9 DEMs and 872 mRNAs were selected after filtering. Then, target genes were uploaded to Metascape to construct protein-protein interaction (PPI) network. Also, 6 hub mRNAs were screened after performing the PPI network. Furthermore, a total of 4 out of 9 miRNAs had an obvious association with the survival rate (P < 0.05) and showed a good power of risk prediction model of over survival. The present research may provide a deeper understanding of regulatory genes of dabrafenib resistance in melanoma. [ABSTRACT FROM AUTHOR]