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Circulating non-coding RNAs in Huntington disease

ABSTRACT: Circulating non-coding RNAs in Huntington disease

PROVIDER: PRJNA705157 | ENA |

REPOSITORIES: ENA

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Circulating non-coding RNAs in Huntington disease

Project description:We performed a study of whole non-coding RNA expression profiles, by microarray, in plasma from 9 patients with Huntington disease (CH) in early stage and 13 controls: 8 healthy subjects (HD) and 5 patients with schizophrenia (SC). The CH patients were under antipsychotic drugs, the most effective treatment option also in SC patient (we included in the study SC control group to minimize the impact of neuroleptic drugson the expression of non-coding RNAs and to identify a HD-specific set of non-coding RNAs). Blood samples were obtained by venous punctures in EDTA-tubes for plasma preparation. Cell- and platelet-free plasma was prepared following a step centrifugation protocol: samples were centrifuged at 1.500 g for 15′ at 4 °C and supernatant will be stored at −80 °C. RNA was extracted using Plasma/Serum Circulating RNA purification Kit (NORGEN) following the manufacturer’s instructions. Labeled RNA from each sample was analyzed by GeneChipmiRNA 2.0 Array (Affymetrix) according to the manufacturer’s instructions. Raw data were analyzed using Partek Genomic Suite software. Looking for differently expressed non-coding RNAs, we found a candidate HC-specific set compared to both control groups (HD and SC) (p<0.05 and │foldchanges│>1.5): hsa-miR-98 has proved to be down-regulated, while hsa-miR-323b-3p was up-regulated; 2 novel snoRNAs were up-regulated.

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Distinct Expression Profiles of long non-coding RNAs and messenger RNAs in circulating leukocytes of Parkinson’s disease

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Distinct Expression Profiles of long non-coding RNAs and messenger RNAs in circulating leukocytes of Parkinson’s disease

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Relevance study and prognostic analysis for intestinal flora disorders affecting non-coding RNA networks in patients with advanced lung cancer

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The characterization of circulating extracellular vesicles and small non-coding RNAs cargo in idiopathic inflammatory myopathies reveals differences across clinically diagnosed myositis subsets

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Bacterial non-coding RNAs excised from within protein-coding transcripts

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Comprehensive Identification of Soybean Long Non-coding RNAs Reveals a Subset of Small Peptide-Coding Transcripts

Project description:Long non-coding RNAs (lncRNAs) are defined as non-protein-coding transcripts that are at least 200 nucleotides long. They are known to play pivotal roles in regulating gene expression, especially during stress responses in plants. We used a large collection of in-house transcriptome data from various soybean (Glycine max and Glycine soja) tissues treated under different conditions to perform a comprehensive identification of soybean lncRNAs. We also retrieved publicly available soybean transcriptome data that were of sufficient quality and sequencing depth to enrich our analysis. In total, RNA-seq data of 332 samples were used for this analysis. An integrated reference-based, de novo transcript assembly was developed that identified ~69,000 lncRNA gene loci. We showed that lncRNAs are distinct from both protein-coding transcripts and genomic background noise in terms of length, number of exons, transposable element composition, and sequence conservation level across legume species. The tissue-specific and time-specific transcriptional responses of the lncRNA genes under some stress conditions may suggest their biological relevance. The transcription start sites of lncRNA gene loci tend to be close to their nearest protein-coding genes, and they may be transcriptionally related to the protein-coding genes, particularly for antisense and intronic lncRNAs. A previously unreported subset of small peptide-coding transcripts was identified from these lncRNA loci via tandem mass spectrometry, which paved the way for investigating their functional roles. Our results also highlight the current inadequacy of the bioinformatic definition of lncRNA, which excludes those lncRNA gene loci with small open reading frames (ORFs) from being regarded as protein-coding.

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Huntington disease protein accelerates tumour development and metastasis

Project description:Huntington disease is a severe neurological disorder caused by an abnormal polyglutamine expansion in the N-terminal of the huntingtin protein. Here we show that breast tumours appear earlier when mutant huntingtin is expressed in an activated polyomavirus middle T antigen (PyVT) mouse breast cancer model as compared to the control mice expressing wild-type huntingtin. Tumours bearing mutant huntingtin have a modified gene expression pattern revealing increases in the IGF-1/Akt signalling, epithelial-mesenchymal transition and metastatic properties. Indeed, polyQ-huntingtin expressing tumours show hyper-activation of Akt pathway. Also, when mutant huntingtin is expressed, cancer cells in culture change morphology and the levels of cell adhesion and mesenchymal markers are affected in primary tumour or corresponding derived cells. As a consequence, PyVT induced lung metastasis is higher in Huntington disease mice than in the control mice. Finally, analysis of cases of Huntington disease patients developing breast cancer may suggest an increased aggressiveness of breast cancer when compared to the control population. 8 Total samples were analyzed: 4 x MMTV-PyVT/HdhQ7/Q7 breast tumours; 4 x MMTV-PyVT/HdhQ111/Q111 breast tumours;

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