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The long non-coding RNA ELDR suppresses tumorigenicity of AML cell lines with MLL rearrangements by interfering with DNA replication and chromatin accessibility [ATAC-Seq]

ABSTRACT: ATAC-seq experiments were performed using the C1 and C3 stable ELDR overexpressing THP1 cell lines, an empty vector control cell line (EV) and non-transfected THP-1 cell (NT). The ATAC-seq experiment was done with two replicas for the two ELDR lines C1 and C3, EV- and NT control each.

ORGANISM(S): Homo sapiens

PROVIDER: GSE273382 | GEO | 2025/12/31

REPOSITORIES: GEO

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The long non-coding RNA ELDR suppresses tumorigenicity of AML cell lines with MLL rearrangements by interfering with DNA replication and chromatin accessibility [RNA-Seq]

Project description:RNA-seq analysis comparing the transcription of stable ELDR overexpressing THP-1 lines (C1 and C3) with empty vector (EV) controls.

2025-12-31 | GSE273380 | GEO

Long non-coding RNA ELDR promotes cell cycle progression in normal oral keratinocytes through induction of a CTCF-FOXM1-AURKA signaling axis

Project description:Long non-coding RNAs (lncRNAs) have gained widespread attention as a potential new layer of regulation in biological processes during development and disease. The lncRNA ELDR (EGFR long non‐coding downstream RNA) was recently shown to be highly expressed in oral cancers as compared to adjacent non-tumor tissue, and we previously reported that ELDR may be an oncogene as inhibition of ELDR reduces tumor growth in oral cancer models. Furthermore, overexpression of ELDR induces proliferation and colony formation in normal oral keratinocytes (NOKs). In this study, we examined in further detail how ELDR drives the neoplastic transformation of normal keratinocytes. We performed RNA-seq analysis on NOKs stably expressing ELDR (NOK-ELDR), which revealed that ELDR enhances the expression of cell cycle-related genes. Increased expression of Aurora kinase A (AURKA) and its downstream gene targets Polo-Like Kinase 1 (PLK1), Cell Division Cycle 25C (CDC25C), Cyclin-Dependent Kinase 1 (CDK1), and Cyclin B1 (CCNB1) are significantly increased in NOK-ELDR cells, suggesting induction of G2/M progression. We further identified CCCTC-Binding Factor (CTCF) as a binding partner of ELDR in NOK-ELDR cells. We showed that ELDR stabilizes CTCF and increases its expression. Finally, we demonstrate the ELDR-CTCF axis upregulates transcription factor Forkhead Box M1 (FOXM1), which induces AURKA expression and downstream G2/M transition. These findings provide mechanistic insights into the role of the lncRNA ELDR as a potential driver of oral cancer during neoplastic transformation of normal keratinocytes.

2022-05-11 | GSE198818 | GEO

The long noncoding RNA ELDR serves as an epigenetic driver in aging and injury-induced chondrocyte senescence [chondrocytes part1]

Project description:Using large-scale patient data sets and genetically engineered (inducible conditional knockout and knockin) mouse models, we show that a novel transcript of long noncoding RNA ELDR is essential for the development of chondrocyte senescence.

2021-06-20 | GSE178090 | GEO

The long noncoding RNA ELDR serves as an epigenetic driver in aging and injury-induced chondrocyte senescence [chondrocytes part2]

2021-06-20 | GSE178091 | GEO

Batch wt vs hyper +_- pABA Normal int_Filtered fg-bg2

Project description:Transcriptional analysis upon the overexpression of the folate gene cluster on a high copy plasmid when compared to an empty vector in the lactic acid bacterium L. plantarum. The transcriptional response was determined for both strains in the presence and absence of pABA thereby using the hybridisation sceme as described in the data processing section. Keywords: response to folate gene cluster overexpression and pABA treatment The batch experiment with and without pABA scheme consisted of a loop design with 21 microarrays with the following samples hybridized on one array and labeled with Cy3 and Cy5, respectively: C1+P and F1+P, F1+P and C2+P, C2+P and F3+P, F3+P and C3+P, C3+P and F2+P, F2+P and C1+P, C1+P and C2+P, F2+P and F3+P, C1-P and F1-P, F1-P and C2-P, C2-P and F3-P, F3-P and C3-P, C3-P and F2-P, F2-P and C1-P, C1-P and C2-P, F2-P and F3-P, C3-P and F1+P, F2+P and C1-P, C2+P and F3-P, F1-P and C3+P, and F2+P and F1-P. Here, C1+P, C2+P, C3+P, F1+P, F2+P, and F3+P represent biological triplicates of the L. plantarum harboring pNZ7021 and pNZ7026, respectively, when grown in batch in the presence of pABA. The C1-P, C2-P, C3-P, F1-P, F2-P, and F3-P, represents the L. plantarum harboring pNZ7021 and pNZ7026, respectively, when grown in batch in the absence of pABA.

2008-05-31 | E-GEOD-8956 | biostudies-arrayexpress

Populus deltoides cultivar:EV

Project description:Populus deltoides EV transcriptome - EV C3 leaf

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Populus deltoides cultivar:EV

Project description:Populus deltoides EV transcriptome - EV C3 stem

| PRJNA520096 | ENA

Populus deltoides cultivar:EV

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| PRJNA520082 | ENA

Populus deltoides cultivar:EV

Project description:Populus deltoides EV transcriptome - EV C1 stem

| PRJNA520094 | ENA

SMN2 splicing modifiers improve motor function and longevity in mice with spinal muscular atrophy

Project description:Characterization of the selectivity of SMN splicing modifiers in SMA type I fibroblasts by RNASeq In total 12 samples were analyzed, divided into four distinct groups (treated with SMN-C3 @ 500 nM; controls for SMN-C3; treated with SMN-C1 @ 100 nM; controls for SMN-C1) containing 3 replicates each.

2014-10-22 | E-GEOD-62540 | biostudies-arrayexpress

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