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The Long Non-coding RNA Lnc-RAINY Regulates Genes Involved in Radiation Susceptibility Through DNA:DNA:RNA triplex-forming Interactions and has Tumor Therapeutic Potential in Non-small Cell Lung Cancers [RNA-seq]

ABSTRACT: Lung Cancer is the leading cause of cancer related deaths worldwide. Unfortunately, radiation resistance is a major problem facing lung cancer patients. Recently, we identified a group of long non-coding RNAs (lncRNAs) known as linc-SPRY3 RNAs, expressed from the Y-chromosome, that play a role in radiation sensitivity by decreasing tumor burden in vitro and in vivo after radiation. In this study, we found that the linc-SPRY3 RNAs are one large lncRNA that we named Radiation Induced Y-chromosome linked long non-coding RNA (lnc-RAINY). Through ATAC-Seq and Immunoprecipitation experiments, we show that lnc-RAINY interacts with DNA in a triple helix to change chromatin opening and gene expression. We also identified that lnc-RAINY regulates CDC6 and CDC25A expression affecting the induction of senescence, inhibition in cell migration, and cell cycle regulation. Furthermore, the administration of nanoparticle encapsulated lnc-RAINY into a lung cancer patient-derived xenograft model dramatically reduces tumor progression demonstrating its therapeutic potential.

ORGANISM(S): Homo sapiens

PROVIDER: GSE274485 | GEO | 2025/04/23

REPOSITORIES: GEO

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The Long Non-coding RNA Lnc-RAINY Regulates Genes Involved in Radiation Susceptibility Through DNA:DNA:RNA triplex-forming Interactions and has Tumor Therapeutic Potential in Non-small Cell Lung Cancers [ATAC-seq]

Project description:Lung Cancer is the leading cause of cancer related deaths worldwide. Unfortunately, radiation resistance is a major problem facing lung cancer patients. Recently, we identified a group of long non-coding RNAs (lncRNAs) known as linc-SPRY3 RNAs, expressed from the Y-chromosome, that play a role in radiation sensitivity by decreasing tumor burden in vitro and in vivo after radiation. In this study, we found that the linc-SPRY3 RNAs are one large lncRNA that we named Radiation Induced Y-chromosome linked long non-coding RNA (lnc-RAINY). Through ATAC-Seq and Immunoprecipitation experiments, we show that lnc-RAINY interacts with DNA in a triple helix to change chromatin opening and gene expression. We also identified that lnc-RAINY regulates CDC6 and CDC25A expression affecting the induction of senescence, inhibition in cell migration, and cell cycle regulation. Furthermore, the administration of nanoparticle encapsulated lnc-RAINY into a lung cancer patient-derived xenograft model dramatically reduces tumor progression demonstrating its therapeutic potential.

2025-04-23 | GSE274484 | GEO

Evidence of Y Chromosome LncRNAs involved in Radiation Response of Male Non-Small Cell Lung Cancer Cells

Project description:Numerous studies have implicated changes in the Y chromosome in male cancers, however few have investigated the biological importance of Y chromosome non-coding RNAs. Here, we demonstrate a group of Y chromosome-expressed long non-coding RNAs (lncRNAs) involved in male non-small cell lung cancer (NSCLC) radiation sensitivity. Radiosensitive male NSCLC cell lines demonstrated a dose-dependent induction of linc-SPRY3-2/3/4 following irradiation, not observed in radioresistant male NSCLC cell lines. Cytogenetics revealed the loss of chromosome Y (LOY) in the radioresistant male NSCLC cell lines. Gain- and loss-of-function experiments indicated that linc-SPRY3-2/3/4 transcripts affect cell viability and apoptosis. UV Cross-linking and Immunoprecipitation (CLIP) and RNA stability assays identify IGF2BP3 as a binding partner for the linc-SPRY3-2/3/4 RNAs which alters the half-life of the anti-apoptotic HMGA2 mRNA as well as the oncogenic c-MYC mRNA. To assess the clinical relevance of these findings, we examined the presence of the Y chromosome in NSCLC tissue microarrays and the expression of linc-SPRY3-2/3/4 in NSCLC RNAseq and microarray data. We observed a negative correlation between the loss of the Y chromosome or linc-SPRY3-2/3/4 and overall survival. Thus, linc-SPRY3-2/3/4 expression and LOY could represent an important marker of radiation therapy in NSCLC.

2020-03-30 | GSE147708 | GEO

The human lncRNA LINC-PINT inhibits tumor cell migration through a highly conserved sequence element

Project description:It is now obvious that the majority of cellular transcripts do not code for proteins, and a significant subset of them are long noncoding RNAs (lncRNAs). Many lncRNAs show aberrant expression in cancer, and some of them have been linked to cellular transformation. However, the underlying mechanisms remain poorly understood. Here we characterize the function of the p53-regulated human lncRNA LINC-PINT in cancer. We found that LINC-PINT acts as tumor suppressor lncRNA. Its expression is downregulated in multiple types of cancer and correlates with good prognosis in lung adenocarcinoma. LINC-PINT inhibits the migration capacity and invasive phenotype of cancer cells in vitro and in vivo, and it does so by repressing a proinvasion gene signature in a PRC2-dependent manner. By applying cross-species conservation analysis combined with functional experimental validations we found that the function of LINC-PINT is highly dependent on a short sequence conserved across mammals, sequence that mediates the interaction with PRC2. We propose that LINC-PINT may function as a molecular exchanger that provides PRC2 to active gene promoters for their silencing, mechanisms that could be shared by other PRC2-interacting lncRNAs.

2017-09-27 | GSE98928 | GEO

biotin RNA pulldown assay of lnc-GD2H and mass spectrometry

Project description:Vectors carrying lnc-GD2H and antisense lnc-GD2H were linearized with the corresponding restriction enzymes to prepare template DNAs for in vitro transcription. Biotinylated RNAs were mixed with proteins extracted from C2C12 cells, followed by targeting of the RNAs with streptavidin beads. After SDS-PAGE following RNA pulldown, the differentially expressed proteins were enzymolyzed and used for MS analysis.

2021-05-18 | PXD025292 | Pride

Systematic Analysis of Long Intergenic Non-Coding RNAs in C. elegans Germline Uncovers Roles in Somatic Growth

Project description:Long intergenic non-coding RNAs (lincRNAs) are transcripts longer than 200 nucleotides that are transcribed from non-coding loci yet undergo biosynthesis similar to coding mRNAs. The disproportional number of lincRNAs expressed in testes suggests that lincRNAs are important during gametogenesis, but experimental evidence has implicated very few lincRNAs in this process. We took advantage of the relatively limited number of lincRNAs in the genome of the nematode Caenorhabditis elegans to systematically analyse the functions of lincRNAs during meiosis. We deleted six lincRNA genes that are highly and dynamically expressed in the C. elegans gonad and tested the effects on central meiotic processes. Surprisingly, whereas the lincRNA deletions did not strongly impact fertility, germline apoptosis, crossovers, or synapsis, linc-4 was required for somatic growth. Slower growth was observed in linc-4-deletion mutants and in worms depleted of linc-4 using RNAi, indicating that linc-4 transcripts are required for this post-embryonic process. Unexpectedly, analysis of worms depleted of linc-4 in soma versus germline showed that the somatic role stems from linc-4 expression in germline cells. This unique feature suggests that some lincRNAs, like some small non-coding RNAs, are required for germ-soma interactions

2021-07-31 | GSE154322 | GEO

Long non-coding RNA Linc-RAM enhances myogenic differentiation by interacting with MyoD

Project description:Long non-coding RNAs are important regulators of diverse biological prosesses. Here, we report on functional identification and characterization of a novel long intergenic noncoding RNA with MyoD-regulated and skeletal muscle-restricted expression that promotes the activation of the myogenic program, and is therefore termed Linc-RAM (Linc-RNA Activator of Myogenesis). Linc-RAM is transcribed from an intergenic region of myogenic cells and its expression is upregulated during myogenesis. Notably, in vivo functional studies show that Linc-RAM knockout mice display impaired muscle regeneration due to differentiation defect of satellite cells. Mechanistically, Linc-RAM regulates expression of myogenic genes by directly binding MyoD, which in turn promotes the assembly of the MyoD-Baf60c-Brg1 complex on the regulatory elements of target genes. Collectively, our findings reveal the functional role and molecular mechanism of a lineage-specific Linc-RAM as a regulatory lncRNA required for tissues-specific chromatin remodeling and gene expression.

2016-12-25 | GSE72601 | GEO

E-PROT-143

Project description:Comparison of Lung Cancer Proteome Profiles 3: DIA

2024-06-05 | E-PROT-143 | ExpressionAtlas

E-MTAB-6957

Project description:RNA profiling of non-small cell lung cancer

2025-01-23 | E-MTAB-6957 | ExpressionAtlas

Comprehensive Identification of Long Non-coding RNAs in Purified Cell Types from the Brain Reveals Functional LncRNA in OPC Fate Determination (RNA-Seq of differentiated NSC after lnc-OPC knockdown)

Project description:To quantitative analysis of transcriptome changes caused by lnc-OPC knockdown during OPC differentiation from NSC, lentivirus-based short hairpin RNAs were used to knockdown the lnc-OPC expression in a neural stem cell culture . Subsequently, puromycin-selected NSCs were differentiated to OPC in culture for three days.RNA-Seq was performed on the polyadenylated fraction of RNA isolated from cell samples. DEseq was used for differential gene expression analysis caused by lnc-OPC knockdown. GO functional term enrichment analysis of differential gene expression caused by lnc-OPC knockdown, revealed significant enrichment of âoligodendrocyte developmentâ, âoligodendrocyte differentiationâ, âglia cell developmentâ, and âaxon ensheathmentâ terms that are associated with oligodendrogenesis. mRNA profiles of differentiiated NSC samples after lnc-OPC knockdown by RNA-sequencing.

2015-11-04 | E-GEOD-74647 | biostudies-arrayexpress

De novo Reconstruction of Adipose Tissue Transcriptomes Reveals Novel Long Non-coding RNAs that Regulate Brown Adipocyte Development

Project description:Brown adipose tissue (BAT) protects against obesity by promoting energy expenditure via uncoupled respiration. To uncover BAT-specific long non-coding RNAs (lncRNAs), we used RNA-seq to reconstruct de novo transcriptomes of mouse brown, inguinal white, and epididymal white fat and identified ~1500 lncRNAs, including 127 BAT-restricted loci induced during differentiation and often targeted by key regulators PPARγ, C/EBPα and C/EBPβ. One of them, lnc-BATE1, is required for establishment and maintenance of BAT identity and thermogenic capacity. lnc-BATE1 inhibition impairs concurrent activation of brown fat and repression of white fat genes, and is partially rescued by exogenous lnc-BATE1 with mutated siRNA-targeting sites, demonstrating a function in trans. We show that lnc-BATE1 binds heterogeneous nuclear ribonucleoprotein U and that both are required for brown adipogenesis. Our work provides an annotated catalog for the study of fat depot-selective lncRNAs, available online, and establishes lnc-BATE1 as a novel regulator of BAT development and physiology. Total RNA profiles of BAT, iWAT and eWAT samples were sequenced on the Illumina HiSeq2000 platform

2015-04-23 | E-GEOD-66686 | biostudies-arrayexpress

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