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

ABSTRACT: Proteome analysis of Biotin- PLANE pull-down assays

ORGANISM(S): Homo Sapiens

SUBMITTER: Xudong Zhang

PROVIDER: PXD022747 | iProX | Thu Nov 26 00:00:00 GMT 2020

REPOSITORIES: iProX

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The pan-cancer lncRNA PLANE regulates an alternative splicing program to promote cancer pathogenesis.

Teng Liu L Feng Yu Chen YC Guo Su Tang ST Wang Pei Lin PL Qi Teng Fei TF Yue Yi Meng YM Wang Shi Xing SX Zhang Sheng Nan SN Tang Cai Xia CX La Ting T Zhang Yuan Yuan YY Zhao Xiao Hong XH Gao Jin Nan JN Wei Li Yuan LY Zhang Didi D Wang Jenny Y JY Shi Yujie Y Liu Xiao Ying XY Li Jin Ming JM Cao Huixia H Liu Tao T Thorne Rick F RF Jin Lei L Shao Feng-Min FM Zhang Xu Dong XD

Nature communications 20210618 1

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 ...[more]

PMID: 34145290

Similar Datasets

The pan-cancer lncRNA PLANE regulates an alternative splicing program to promote cancer pathogenesis.

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.

| S-EPMC8213729 | biostudies-literature

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

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.

2020-11-27 | GSE162215 | GEO

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

2021-04-16 | GSE172124 | GEO

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

Project description:The pan-cancer lncRNA PLANE regulates an alternative splicing program and promotes cancer pathogenesis

| PRJNA681019 | ENA

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

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

| PRJNA722174 | ENA

A lncRNA regulates alternative splicing via establishment of a splicing-specific chromatin signature.

Project description:Alternative pre-mRNA splicing is a highly cell type-specific process essential to generating protein diversity. However, the mechanisms responsible for the establishment and maintenance of heritable cell-specific alternative-splicing programs are poorly understood. Recent observations point to a role of histone modifications in the regulation of alternative splicing. Here we report a new mechanism of chromatin-mediated splicing control involving a long noncoding RNA (lncRNA). We have identified an evolutionarily conserved nuclear antisense lncRNA, generated from within the human FGFR2 locus, that promotes epithelial-specific alternative splicing of FGFR2. The lncRNA acts through recruitment of Polycomb-group proteins and the histone demethylase KDM2a to create a chromatin environment that impairs binding of a repressive chromatin-splicing adaptor complex important for mesenchymal-specific splicing. Our results uncover a new function for lncRNAs in the establishment and maintenance of cell-specific alternative splicing via modulation of chromatin signatures.

| S-EPMC6322542 | biostudies-literature

c-Myc inactivation of p53 through the pan-cancer lncRNA MILIP drives cancer pathogenesis.

Project description:The functions of the proto-oncoprotein c-Myc and the tumor suppressor p53 in controlling cell survival and proliferation are inextricably linked as "Yin and Yang" partners in normal cells to maintain tissue homeostasis: c-Myc induces the expression of ARF tumor suppressor (p14ARF in human and p19ARF in mouse) that binds to and inhibits mouse double minute 2 homolog (MDM2) leading to p53 activation, whereas p53 suppresses c-Myc through a combination of mechanisms involving transcriptional inactivation and microRNA-mediated repression. Nonetheless, the regulatory interactions between c-Myc and p53 are not retained by cancer cells as is evident from the often-imbalanced expression of c-Myc over wildtype p53. Although p53 repression in cancer cells is frequently associated with the loss of ARF, we disclose here an alternate mechanism whereby c-Myc inactivates p53 through the actions of the c-Myc-Inducible Long noncoding RNA Inactivating P53 (MILIP). MILIP functions to promote p53 polyubiquitination and turnover by reducing p53 SUMOylation through suppressing tripartite-motif family-like 2 (TRIML2). MILIP upregulation is observed amongst diverse cancer types and is shown to support cell survival, division and tumourigenicity. Thus our results uncover an inhibitory axis targeting p53 through a pan-cancer expressed RNA accomplice that links c-Myc to suppression of p53.

| S-EPMC7536215 | biostudies-literature

Alternative splicing modulation mediated by G-quadruplex structures in MALAT1 lncRNA

Project description:MALAT1, an abundant lncRNA specifically localized to nuclear speckles, regulates alternative-splicing (AS). The molecular basis of its role in AS remains poorly understood. Here, we report three conserved, thermodynamically stable, parallel RNA-G-quadruplexes (rG4s) present in the 3’ region of MALAT1 which regulates this function. Using rG4 domain specific RNA-pull-down followed by mass-spectrometry, RNA-immuno-precipitation and imaging, we demonstrate the rG4 dependent localization of Nucleolin (NCL) and Nucleophosmin (NPM) to nuclear speckles. Specific G-to-A mutations that abolish rG4 structures, results in the localization loss of both the proteins from speckles. Functionally, disruption of rG4 in MALAT1 phenocopies NCL knockdown resulting in altered pre-mRNA splicing of endogenous genes. These results reveal a central role of rG4s within the 3’ region of MALAT1 orchestrating AS.

2022-02-17 | PXD026386 | Pride

LncRNA Ctcflos orchestrates transcription and alternative splicing in thermogenic adipogenesis

Project description:The recruitment of thermogenic brite adipocytes within white adipose tissue attenuates obesity and metabolic comorbidities, arousing interest in understanding the underlying regulatory mechanisms. The molecular network of brite adipogenesis, however, remains largely unresolved. In this light, long noncoding RNAs (lncRNAs) emerged as a versatile class of modulators that control many steps within the differentiation machinery. Leveraging the naturally varying propensities of different inbred mouse strains for white adipose tissue browning, we identify the nuclear lncRNA Ctcflos as a pivotal orchestrator of thermogenic gene expression during brite adipocyte differentiation. Mechanistically, Ctcflos acts as a bi-functionalpleiotropic regulator, being essential for the transcriptional recruitment of the early core thermogenic regulatory program and the modulation of alternative splicing to drive brite adipogenesis. This is showcased by Ctcflos regulated gene transcription and splicing of the key browning factor Prdm16 towards its isoform that is specific for the thermogenic gene program. Conclusively, our findings emphasize the mechanistic versatility of lncRNAs acting at several independent levels of gene expression for effective regulation of key differentiation factors to direct cell fate and function.

| S-SCDT-EMBOR-2020-51289V1 | biostudies-other

Survival-Associated Alternative Splicing Events in Pan-Renal Cell Carcinoma.

Project description:Alternative splicing is an important modification process for the genome to generate mature mRNA by transcription, which has been found associated with survival in some tumors. However, systematic analysis of AS events in pan-renal cell carcinoma at the genome-wide level has been seldom conducted yet. In the current study, Upset plot and Venn plot were utilized to present the distribution characteristics of AS events. Those SREs were screened out with multivariate COX regression analyses, and functional enrichment analysis was performed to figure out potential pathways. ROC model was conducted to compare the efficiency of those potential SREs. A total of 2,169, 1,671, and 1,414 SREs were found in renal clear cell carcinoma (KIRC), renal chromophobe cell carcinoma (KICH), and renal papillary cell carcinoma (KIRP), respectively. Functional enrichment analysis results suggested possible mechanism such as changes in the branched-chain amino acid catabolic process due to SREs might play a key role in KIRC. The binary logistic regression equation based on the SREs had a good performance in each model compared to the single factor. The 5 year survival model presented that the AUC of the predicted probabilities in KIRC, KICH, and KIRP were 0.754, 1 and 0.841, and in the diagnostic model were 0.988, 0.970, and 0.999, respectively. Some AS types that were significantly different in pan-RCC and paracancerous tissues have also been discovered to play a role in carcinoma screening. To sum up, alternative splicing events significantly interfere with the prognosis of patients with pan-RCC and are capable as biomarkers for prognosis.

| S-EPMC6902018 | biostudies-literature

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