Pervasive Chromatin-RNA Binding Protein Interactions Enable RNA-Based Regulation of Transcription

Rheumatoid arthritis (RA) is a chronic autoimmune disease of unknown etiology, mainly manifested by persistent abnormal proliferation of fibroblast-like synoviocytes (FLSs), inflammation, synovial hyperplasia and cartilage erosion, accompanied by joint swelling and joint destruction. Abnormal expression or function of long noncoding RNAs (lncRNAs) are closely related to human diseases, including cancers, mental diseases, autoimmune diseases and others. The abnormal sequence and spatial structure of lncRNAs, the disorder expression and the abnormal interaction with the binding protein will lead to the change of gene expression in the way of epigenetic modification. Increasing evidence demonstrated that lncRNAs were involved in the activation of FLSs, which played a key role in the pathogenesis of RA. In this review, the research progress of lncRNAs in the pathogenesis of RA was systematically summarized, including the role of lncRNAs in the diagnosis of RA, the regulatory mechanism of lncRNAs in the pathogenesis of RA, and the intervention role of lncRNAs in the treatment of RA. Furthermore, the activated signal pathways, the role of DNA methylation and other mechanism have also been overview in this review.

/pdf/dysregulation-of-lncrnas-in-rheumatoid-arthritis-biomarkers-4pomv37t7m.pdf

Dysregulation of lncRNAs in Rheumatoid Arthritis: Biomarkers, Pathogenesis and Potential Therapeutic Targets.

Accumulating evidences indicate that long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) promotes the progression of glioma. In this study, we postulated that NEAT1 may act as a miR-128-3p sponge. Relative levels of NEAT1 and miR-128-3p expression in human glioma samples and GBM cells were detected using quantitative real-time PCR. By means of CCK-8 assays, transwell assays, and flow cytometric analysis, the biological functions of miR-128-3p and NEAT1 were investigated in U87MG and U251MG human GBM cell lines with stable miR-128-3p and NEAT1 knockdown or overexpression. The luciferase reports, RNA pull-down assay, and RNA immunoprecipitation assay were conducted to determine the relevance of NEAT1 and miR-128-3p in glioma. As a result, high expression of NEAT1 and lack of miR-128-3p were observed in glioma specimens and cells. By binding to anti-oncogene miR-128-3p in the nucleus, NEAT1 enhanced tumorigenesis and glioma development. Further experiments suggested that ITGA5 expression was increased in glioma tissues and was found to be connected with miR-128-3p. Additionally, NEAT1 facilitated ITGA5 expression via competitively binding to miR-128-3p. For this reason, ITGA5 would not be decomposed by miR-128-3p and could activate FAK signaling pathway, thereby promoting cell growth. Collectively, these results indicated that the NEAT1/miR-128-3p/ITGA5 axis was involved in glioma initiation and progression, and might offer a potential novel strategy for treatment of glioma.

/pdf/lncrna-neat1-enhances-glioma-progression-via-regulating-the-2lrfx8jyrb.pdf

LncRNA NEAT1 Enhances Glioma Progression via Regulating the miR-128-3p/ITGA5 Axis

Hypertrophic Scar (HS) is a complicated fibrotic disease In addition, its pathogenesis is still to be further explored Long non-coding RNAs (lncRNAs) have been proved to be participated in multiple diseases, including HS However, the role of lncRNA TUG1 in HS remains unclear The expression level of RNA and protein in cells were detected by q-PCR and western blot, respectively MTT assay was performed to test the cell proliferation Cell migration was detected by transwell assay Cell apoptosis was measured by flow cytometry Dual luciferase report assay and RNA pull down were used to verify the relationship between TUG1, miR-27b-3p and TAK1TUG1 and TAK1 were upregulated in HS, while miR-27b-3p was downregulated Knockdown of TUG1 significantly suppressed the proliferation and migration and induced the apoptosis of HS fibroblasts (HSF) In addition, silencing of TUG1 notably inhibited the extracellular matrix (ECM) biosynthesis in HSF Overexpression of miR-27b-3p has the same effect on HS as that of TUG1 knockdown Meanwhile, TUG1 could sponge miR-27b-3p, and TAK1 was the direct target of miR-27b-3p Furthermore, knockdown of TUG1 significantly suppressed the fibrosis in HS via miR-27b-3p/TAK1/YAP/TAZ axis mediation LncRNA TUG1 promotes the fibrosis in HS via sponging miR-27b-3p and then activates TAK1/YAP/TAZ pathway, which may serve as a potential target for treatment of HS

LncRNA TUG1 exhibits pro-fibrosis activity in hypertrophic scar through TAK1/YAP/TAZ pathway via miR-27b-3p.

Objective: This study aims to determine the expression pattern of long non-coding RNA (lncRNA) TUSC8 in esophageal cancer tissues and cell lines, to investigate its effects on esophageal cancer cell proliferation and migration, and to explore the mechanism of TUSC8-mediated esophageal cancer suppression via VEGFA downregulation. Patients and Methods: TUSC8 levels in esophageal cancer tissues and cell lines were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The influence of TUSC8 on clinical features in esophageal cancer patients was analyzed. After intervening TUSC8 expression in esophageal cancer cells, the proliferative and migratory abilities were examined in OE19 and TE-1 cells through a series of function experiments. The interaction between TUSC8 and VEGFA was assessed by the bioinformatics prediction and dual-luciferase reporter assay. Finally, the co-regulation of TUSC8 and VEGFA on esophageal cancer cell functions was evaluated. Results: TUSC8 was downregulated in esophageal cancer tissues compared with normal ones. Identically, decreased TUSC8 expression was detected in esophageal cancer cell lines compared with control cells. Low TUSC8 expression predicted poor prognosis in patients with esophageal cancer. Knockdown of TUSC8 promoted the proliferative and migratory abilities in OE19 cells, whereas overexpression of TUSC8 resulted in opposite results in TE-1 cells. VEGFA was confirmed to be a target gene of TUSC8. Overexpression of VEGFA could reverse the regulatory effects of TUSC8 on esophageal cancer cell proliferation and migration. Conclusions: LncRNA TUSC8 is downregulated in esophageal cancer tissues and cell lines. TUSC8 inhibits the proliferative and migratory abilities in esophageal cancer cells in vitro by negatively regulating VEGFA.

/pdf/lncrna-tusc8-suppresses-the-proliferation-and-migration-of-4dalwrws35.pdf

LncRNA TUSC8 suppresses the proliferation and migration of esophageal cancer cells by downregulation of VEGFA

The nucleus is a highly organized and dynamic environment where regulation and coordination of processes such as gene expression and DNA replication are paramount. In recent years, noncoding RNAs have emerged as key participants in the regulation of nuclear processes. There are a multitude of functional roles for long noncoding RNA (lncRNA), mediated through their ability to act as molecular scaffolds bridging interactions with proteins, chromatin, and other RNA molecules within the nuclear environment. In this review, we discuss the diversity of techniques that have been developed to probe the function of nuclear lncRNAs, along with the ways in which those techniques have revealed insights into their mechanisms of action. Foundational observations into lncRNA function have been gleaned from molecular cytology-based, single-cell approaches to illuminate both the localization and abundance of lncRNAs in addition to their potential binding partners. Biochemical, extraction-based approaches have revealed the molecular contacts between lncRNAs and other molecules within the nuclear environment and how those interactions may contribute to nuclear organization and regulation. Using examples of well-studied nuclear lncRNAs, we demonstrate that the emerging functions of individual lncRNAs have been most clearly deduced from combined cytology and biochemical approaches tailored to study specific lncRNAs. As more functional nuclear lncRNAs continue to emerge, the development of additional technologies to study their interactions and mechanisms of action promise to continually expand our understanding of nuclear organization, chromosome architecture, genome regulation, and disease states.

/pdf/probing-the-function-of-long-noncoding-rnas-in-the-nucleus-sse3udiifv.pdf

Probing the function of long noncoding RNAs in the nucleus

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

Velleca Aj

Author Tools

Chat about Author

Papers

Probing the function of long noncoding RNAs in the nucleus