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

ABSTRACT: The long noncoding RNA ELDR serves as an epigenetic driver in aging and injury-induced chondrocyte senescence

PROVIDER: PRJNA737345 | ENA |

REPOSITORIES: ENA

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

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 | GSE178091 | GEO

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

2021-06-20 | GSE178090 | GEO

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

Project description:The long noncoding RNA ELDR serves as an epigenetic driver in aging and injury-induced chondrocyte senescence [lncRNA]

| PRJNA728062 | ENA

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

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

| PRJNA737348 | ENA

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

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

| PRJNA737349 | ENA

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

Project description:To investigate lncRNA profile in OA patients and analyze the critical role of lncRNA in chondrocyte senescence To investigate lncRNA profile in OA patients and analyze the critical role of lncRNA in chondrocyte senescence

2021-06-20 | GSE174049 | 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

Dynamic chromatin accessibility tuning of long noncoding RNA ELDR accelerates chondrocyte senescence and osteoarthritis

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-06-20 | GSE178092 | GEO

Sirt6 attenuates chondrocyte senescence and osteoarthritis progression

Project description:Sirt6 attenuates chondrocyte senescence and osteoarthritis progression

2022-11-29 | GSE206513 | GEO

The UFM1 System Alleviated Fatty Acid Oxidation and Chondrocyte Senescence via the UFMylation of CAVIN1

Project description:Osteoarthritis (OA) is a widespread age-related joint disease caused by the gradual loss of chondrocyte function along with age. Here, we found that UFMylation modification was lower-leveled in senescent cartilage, mediated chondrocyte senescence and OA phenotypes through targeting CAVIN1, which acted as a stimulator in chondrocyte senescence, mainly through promoting CPT1 expression and activating fatty acid β-oxidation (FAO). Physiologically, FAO was at a very low level in chondrocytes, while the anomalous activation of FAO accelerated chondrocyte senescence. UFMylation of CAVIN1 promoted its binding with TRIP12, leading to ubiquitination degradation. Therefore, UFMylation played a pivotal role in post-translationally modification of CAVIN1. Polymeric micellar nanoparticles (NPs) conjugated with UFM1 improved the stability of UFM1 recombinant protein (UFM1-rp), and extended the retention time of UFM1-rp in the mouse joint cavity. The administration of UFM1 into mouse joints using an advanced NP delivery system is effective in attenuating age-related pathogenesis. Therefore, we uncovered a previously unknown mechanism, UFM1-CAVIN1-CPT1 axis, in the protection of OA progression and constructed a new drug for OA treatment, and have provided important preliminary evidence toward the translation of our findings into clinical usage.

2024-04-22 | GSE264185 | GEO

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