scholarly journals Aberrant expression of long non-coding RNA in thyroid neoplasms

2019 ◽  
pp. 17-25
Author(s):  
В.Д. Якушина ◽  
А.С. Танас ◽  
А.В. Лавров
Keyword(s):  
Thyroid Cancer ◽  
Signaling Pathway ◽  
In Silico ◽  
Thyroid Nodules ◽  
Differentially Expressed ◽  
Follicular Variant ◽  
Aberrant Expression ◽  
Lncrna Expression ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Актуальность. Длинные некодирующие РНК (днРНК) при раке щитовидной железы плохо изучены; не известны днРНК, общие и специфичные для фолликулярного и классического вариантов папиллярного рака, не установлены днРНК, аберрантно экспрессированные при других основных субтипах злокачественных новообразований щитовидной железы, а также при доброкачественных новообразованиях. Цель исследования - определить днРНК, аберрантно экспрессированные при фолликулярной аденоме (ФА), фолликулярном раке (ФРЩЖ), фолликулярном и классическом вариантах папиллярного рака (ПРЩЖ), анапластическом раке (АРЩЖ) щитовидной железы. Методы. Проанализирована экспрессия днРНК по данным исследований на микрочипах (8 независимых экспериментов, доступных в GEO) и секвенирования РНК (PRJEB11591 и TCGA-THCA). Исследованы 246 образцов нормальной ткани щитовидной железы, 26 - ФА, 30 - ФРЩЖ, 181 - фолликулярного варианта ПРЩЖ, 481 - классического варианта ПРЩЖ и 49 - АРЩЖ. Для классического и фолликулярного вариантов ПРЩЖ выполнена валидация дифференциальной экспрессии in silico. Потенциальные биологические функции были оценены в результате анализа обогащения коэкспрессированных генов. Результаты. Определены днРНК, дифференциально экспрессированные при ФА, ФРЩЖ, фолликулярном и классическом вариантах ПРЩЖ и АРЩЖ. Выявлены 8 днРНК, экспрессия которых изменена во всех субтипах новообразований щитовидной железы, 22 - общих для ПРЩЖ, 32 - специфичных для классического варианта ПРЩЖ, 1 - специфичная для фолликулярного варианта ПРЩЖ, и 177 - специфичных для АРЩЖ. Статистически значимо дифференциально экспрессированных днРНК в ФРЩ по сравнению с ФА не выявлено. Ранее известные онкогенные и супрессорные днРНК NR2F1-AS1, LINC00511, SLC26A4-AS1, CRNDE, RMST впервые обнаружены в новообразованиях щитовидной железы. Выявленные днРНК предположительно вовлечены в клеточную адгезию, организацию экстрацеллюлярного матрикса, образование эндодермы, регуляцию клеточного цикла и митоза, полярности клеток, сигнальные пути VEGF и WNT. Выводы. Установлены общие и специфичные паттерны экспрессии днРНК в доброкачественных и злокачественных новообразованиях щитовидной железы. Background. Long non-coding RNA (lncRNA) in thyroid cancer are poorly investigated; no lncRNAs common and specific for the follicular and classical variants of papillary cancer, as well as no lncRNAs aberrantly expressed in benign nodules or other subtypes of thyroid cancer are established. The objective of the study is to determine long noncoding RNAs aberrantly expressed in follicular adenoma (FA), follicular carcinoma (FTC), follicular and classical variants of papillary carcinoma (PTC), anaplastic carcinoma (ATC). Methods. lncRNA expression was analyzed in dataset of Microarray (8 independent experiments available in GEO) and RNA-seq studies (PRJEB11591 and TCGA-THCA). In total, 246 samples of normal thyroid tissue, 26 FAs, 30 FTCs, 181 follicular variant PTCs, 481 classic variant PTCs and 49 ATCs were examined. In silico validation was performed. Potential biological functions were assessed by enrichment analysis of coexpressed genes. Results. LncRNAs differentially expressed in FA, FTC, follicular, and classical variants of PTC, and ATC are identified. There are 8 lncRNAs common for all investigated thyroid nodules, 22 common for PTC, 32 specific for classical PTC, 1 specific for follicular variant of PTC, and 177 specific for ATC. No lncRNA significantly differentially expressed in FTC compared to FA is identified. The previously described oncogenic and suppressor lncRNAs NR2F1-AS1, LINC00511, SLC26A4-AS1, CRNDE, RMST are detected in thyroid carcinomas for the first time. Identified lncRNA are putatively involved in cell adhesion, extracellular matrix organization, endoderm formation, VEGF signaling pathway, WNT signaling pathway and cell polarity, cell cycle and mitosis. Conclusion. The general and specific patterns of lncRNA expression in benign and malignant thyroid nodules are established.

scholarly journals Characterization of Long Non-coding RNA Profile in RD and SH-SY5Y Cells Infected by CV-B5 using RNA Sequencing

2021 ◽  
Author(s):  
Wei Chen ◽  
Peiying Teng ◽  
Heng Yang ◽  
Jing Li ◽  
Fan Yang
Keyword(s):  
Signaling Pathway ◽  
Rna Sequencing ◽  
Expression Profiles ◽  
Wnt Signaling Pathway ◽  
Foot And Mouth Disease ◽  
Differentially Expressed ◽  
Host Interactions ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Hand, foot, and mouth disease caused by Coxsackievirus B5 (CV-B5) poses considerable threats to the health of infants especially in neurological damage. And the long noncoding RNAs (lncRNAs) act pivotal factors in regulating and participating in virus-host interactions. However, the role of lncRNAs in CV-B5-host interactions has not yet been elucidated. In this study, we used the RNA sequencing to determine the expression profiles of lncRNAs in CV-B5 infected human rhabdomyosarcoma (RD) and SH-SY5Y cells. Our results identified that in the differentially expressed lncRNAs a total of 508 up-regulated and 760 down-regulated lncRNAs in RD cell, with 46.2% were lincRNAs, 28.6% were anti-sense lncRNAs, 24.1% were sense overlapping lncRNAs, and 1.0% were sense intronic lncRNAs. Moreover, 792 lncRNAs were significantly increased and 811 lncRNAs were greatly decreased in SH-SY5Y cell including 48.6% were lincRNAs, 34.7% were anti-sense lncRNAs, 16.0% were sense overlapping lncRNAs, and 0.8% were sense intronic lncRNAs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway showed that the differentially expressed lncRNAs participated in the occurrence of disease in RD cell and associated with signaling pathway in SH-SY5Y cell after CVB5 infection respectively. In addition, similar results were obtained when seven lncRNAs were selected for validation using RT-qPCR assays. Moreover, we conducted the candidate lncRNA-IL12A secondary structures and found that it inhibits viral replication through Wnt signaling pathway. Our results reveal that lncRNAs can become a possible novel molecular target for the prevention and treatment of CV-B5 infection, and provided information for distinguishing neurogenic CV-B5 disease.

Long non-coding RNA expression profiles in neutrophils revealed potential biomarker for prediction of renal involvement in SLE patients

Rheumatology ◽  
2020 ◽  
Author(s):  
Bin Cai ◽  
Jingyi Cai ◽  
Zhihua Yin ◽  
Xiaoyue Jiang ◽  
Chao Yao ◽  
...  
Keyword(s):  
Disease Activity ◽  
Expression Profiles ◽  
Quantitative Polymerase Chain Reaction ◽  
Renal Involvement ◽  
Differentially Expressed ◽  
Healthy Controls ◽  
Lncrna Expression ◽  
Non Coding Rna ◽  
Potential Biomarker ◽  
Long Non Coding Rna

Abstract Objective The long non-coding RNA plays an important role in inflammation and autoimmune diseases. The aim of this study is to screen and identify abnormally expressed lncRNAs in peripheral blood neutrophils of SLE patients as novel biomarkers and to explore the relationship between lncRNAs levels and clinical features, disease activity and organ damage. Methods RNA-seq technology was used to screen differentially expressed lncRNAs in neutrophils from SLE patients and healthy donors. Based on the results of screening, candidate lncRNA levels in neutrophils of 88 SLE patients, 35 other connective disease controls, and 78 healthy controls were qualified by real-time quantitative polymerase chain reaction. Results LncRNA expression profiling revealed 360 up-regulated lncRNAs and 224 down-regulated lncRNAs in neutrophils of SLE patients when compared with healthy controls. qPCR assay validated that the expression of Lnc-FOSB-1:1 was significantly decreased in neutrophils of SLE patients when compared with other CTD patients or healthy controls. It correlated negatively with SLE Disease Activity Index 2000 (SLEDAI-2K) score (r = −0.541, P < 0.001) and IFN scores (r = −0.337, P = 0.001). More importantly, decreased Lnc-FOSB-1:1 expression was associated with lupus nephritis. Lower baseline Lnc-FOSB-1:1 level was associated with higher risk of future renal involvement (within an average of 2.6 years) in patients without renal disease at baseline (P = 0.019). Conclusion LncRNA expression profile in neutrophils of SLE patients revealed differentially expressed lncRNAs. Validation study on Lnc-FOSB-1:1 suggest that it is a potential biomarker for prediction of near future renal involvement.

scholarly journals Autophagy-Related Long Non-coding RNA Signature as Indicators for the Prognosis of Uveal Melanoma

2021 ◽  
Vol 12 ◽  
Author(s):  
Yi Cui ◽  
Mi Zheng ◽  
Jing Chen ◽  
Nuo Xu
Keyword(s):  
High Risk ◽  
Signaling Pathway ◽  
Uveal Melanoma ◽  
Killer Cell ◽  
Differentially Expressed ◽  
Receptor Signaling ◽  
Regression Analyses ◽  
Non Coding Rna ◽  
Receptor Signaling Pathway ◽  
Long Non Coding Rna

This study aimed to develop an autophagy-associated long non-coding RNA (lncRNA) signature to predict the prognostic outcomes of uveal melanoma (UM). The data of UM from The Cancer Genome Atlas (TCGA) were enrolled to obtain differentially expressed genes (DEGs) between metastasizing and non-metastasizing UM patients. A total of 13 differentially expressed autophagy genes were identified and validated in Gene Expression Omnibus, and 11 autophagy-related lncRNAs were found to be associated with overall survival. Through performing least absolute shrinkage and selection operator regression analyses, a six-autophagy-related lncRNA signature was built, and its efficacy was confirmed by receiver-operating characteristic, Kaplan–Meier analysis, and univariate and multivariate Cox regression analyses. A comprehensive nomogram was established and its clinical net benefit was validated by decision curve analysis. GSEA revealed that several biological processes and signaling pathways including Toll-like receptor signaling pathway, natural killer cell-mediated cytotoxicity, and B- and T-cell receptor signaling pathway were enriched in the high-risk group. CIBERSORT results showed that the signature was related to the immune response especially HLA expression. This signature could be deployed to assist clinicians to identify high-risk UM patients and help scientists to explore the molecular mechanism of autophagy-related lncRNAs in UM pathogenesis.

scholarly journals TMIC-28. LONG NON-CODING RNA EXPRESSION DIFFERS BETWEEN GLIOBLASTOMA PATIENT IMMUNE CELLS AND HEALTHY VOLUNTEERS

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi253-vi253
Author(s):  
Anthony Nwankwo ◽  
Victoria Sanchez ◽  
John Lynes ◽  
Xiang Wang ◽  
Gifty Dominah ◽  
...  
Keyword(s):  
T Cells ◽  
Differential Expression ◽  
Immune Cells ◽  
Fold Change ◽  
Differentially Expressed ◽  
Preliminary Review ◽  
Lncrna Expression ◽  
Glioblastoma Patient ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract To improve glioblastoma treatment, improved characterization of the tumor’s immune microenvironment is critical. Aberrant long non-coding RNA (LncRNA) expression has been implicated in the pathogenesis of many cancers, including glioblastoma. Other studies have discovered long non-coding RNAs which regulate immunity. However, lncRNA expression has not been systematically investigated glioblastoma patient immune cells. We aimed to investigate the differential expression of LncRNA and mRNs in the T lymphocytes and monocytes of glioblastoma patients when compared to healthy controls in an unbiased fashion. CD3 and CD14 cells were sorted from PBMC samples from 3 newly diagnosed glioblastoma patients and 3 normal donors, and RNA was extracted from them. These RNA samples were run on the Arraystar Human LncRNA microarray. We found 309 LncRNAs differentially expressed in glioblastoma patient T cells, and 316 in patient monocytes (fold change >2 or £0.5, P£0.05). A preliminary review of this data has revealed upregulation of lncRNAs that have previously been reported to play a role in tumorigenesis, such as MIF12-AS1, VIM-AS1, and WEE2-AS1. Additionally, lncRNAs such as CCDC26 and Hoxa10 that have been implicated in immune cell differentiation and hyperactivity also show differential expression between the two groups. We also found differential expression of 203 mRNA in T cells and 467 in monocytes (fold change ³2 or £0.5, P£0.05). An analysis based on the Kyoto Encyclopedia of Genes and Genomes identified 42 biological pathways that have enrichment of these differentially expressed mRNAs (P£0.05), including the RIG-I-like receptor pathway and toll-like receptor pathway, both implicated in innate immunity in T-cells. This array data will form the template for future single-cell RNA sequencing of tumor-infiltrating immune cells; peripheral immune cells from glioblastoma patients; and immune cells from non-tumorous brain (epilepsy tissue) and blood samples to investigate these differences in greater detail.

scholarly journals Long non-coding RNA TUG1 knockdown hinders the tumorigenesis of multiple myeloma by regulating the microRNA-34a-5p/NOTCH1 signaling pathway

2020 ◽  
Vol 15 (1) ◽  
pp. 284-295
Author(s):  
Yongtian Zhang ◽  
Dandan Zhao ◽  
Shumei Li ◽  
Meng Xiao ◽  
Hongjing Zhou ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Signaling Pathway ◽  
Notch Receptor ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Notch1 Signaling ◽  
Non Coding Rna ◽  
Notch1 Signaling Pathway ◽  
Long Non Coding Rna

AbstractMultiple myeloma (MM) is a serious health issue in hematological malignancies. Long non-coding RNA taurine-upregulated gene 1 (TUG1) has been reported to be highly expressed in the plasma of MM patients. However, the functions of TUG1 in MM tumorigenesis along with related molecular basis are still undefined. In this study, increased TUG1 and decreased microRNA-34a-5p (miR-34a-5p) levels in MM tissues and cells were measured by the real-time quantitative polymerase reaction assay. The expression of relative proteins was determined by the Western blot assay. TUG1 knockdown suppressed cell viability, induced cell cycle arrest and cell apoptosis in MM cells, as shown by Cell Counting Kit-8 and flow cytometry assays. Bioinformatics analysis, luciferase reporter assay, and RNA pull-down assay indicated that miR-34a-5p was a target of TUG1 and directly bound to notch receptor 1 (NOTCH1), and TUG1 regulated the NOTCH1 expression by targeting miR-34a-5p. The functions of miR-34a-5p were abrogated by TUG1 upregulation. Moreover, TUG1 loss impeded MM xenograft tumor growth in vivo by upregulating miR-34a-5p and downregulating NOTCH1. Furthermore, TUG1 depletion inhibited the expression of Hes-1, Survivin, and Bcl-2 protein in MM cells and xenograft tumors. TUG1 knockdown inhibited MM tumorigenesis by regulating the miR-34a-5p/NOTCH1 signaling pathway in vitro and in vivo, deepening our understanding of the TUG1 function in MM.

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