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The pan-cancer lncRNA PLANE regulates an alternative splicing program and promotes cancer pathogenesis [ONT]

ABSTRACT: The pan-cancer lncRNA PLANE regulates an alternative splicing program and promotes cancer pathogenesis [ONT]

PROVIDER: PRJNA722174 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14243140_1.fastq.gz	Fastqsanger.gz
	SRR14243141_1.fastq.gz	Fastqsanger.gz
	SRR14243142_1.fastq.gz	Fastqsanger.gz
	SRR14243143_1.fastq.gz	Fastqsanger.gz

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The pan-cancer lncRNA PLANE regulates an alternative splicing program and promotes cancer pathogenesis [ONT]

Project description:Genomic amplification of the distal portion of chromosome 3q that encodes a number of oncogenic proteins is one of the most prevalent chromosomal deformities. Here we functionally characterise a non-protein product of this region, the long noncoding RNA (lncRNA) PLANE, which is upregulated in diverse cancer types through copy number gain as well as transcriptional activation by E2F1. PLANE forms an RNA-RNA duplex with the nuclear receptor co-repressor 2 (NCOR2) pre-mRNA at intron 45, binds to heterogeneous ribonucleoprotein M (hnRNPM) and facilitates the association of hnRNPM with the intron, leading to repression of the alternative splicing (AS) event generating NCOR2-202, a major protein-coding NCOR2 AS variant. As such, PLANE promotes cancer cell proliferation and tumorigenicity and its upregulation is associated with poor outcome of patients. These results uncover the function and regulation of PLANE and suggest that PLANE may constitute a therapeutic target in the pan-cancer context.

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Project description:Genomic amplification of the distal portion of chromosome 3q, which encodes a number of oncogenic proteins, is one of the most frequent chromosomal abnormalities in malignancy. Here we functionally characterise a non-protein product of the 3q region, the long noncoding RNA (lncRNA) PLANE, which is upregulated in diverse cancer types through copy number gain as well as E2F1-mediated transcriptional activation. PLANE forms an RNA-RNA duplex with the nuclear receptor co-repressor 2 (NCOR2) pre-mRNA at intron 45, binds to heterogeneous ribonucleoprotein M (hnRNPM) and facilitates the association of hnRNPM with the intron, thus leading to repression of the alternative splicing (AS) event generating NCOR2-202, a major protein-coding NCOR2 AS variant. This is, at least in part, responsible for PLANE-mediated promotion of cancer cell proliferation and tumorigenicity. These results uncover the function and regulation of PLANE and suggest that PLANE may constitute a therapeutic target in the pan-cancer context.

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