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

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

PROVIDER: PRJNA737348 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14803700_1.fastq.gz	Fastqsanger.gz
	SRR14803700_2.fastq.gz	Fastqsanger.gz
	SRR14803701_1.fastq.gz	Fastqsanger.gz
	SRR14803701_2.fastq.gz	Fastqsanger.gz
	SRR14803702_1.fastq.gz	Fastqsanger.gz

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

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

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

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

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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.

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