TGF-beta-upregulated Lnc-Nr6a1 acts as a reservoir of miR-181 and mediates assembly of a glycolytic complex [RNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA857678 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20078505_1.fastq.gz | Fastqsanger.gz | |||
| SRR20078505_2.fastq.gz | Fastqsanger.gz | |||
| SRR20078506_1.fastq.gz | Fastqsanger.gz | |||
| SRR20078506_2.fastq.gz | Fastqsanger.gz | |||
| SRR20078507_1.fastq.gz | Fastqsanger.gz |
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Project description:Long noncoding RNAs (lncRNAs) have emerged as key regulators in a wide range of biological processes. The involvement of lncRNAs in epithelial-to-mesenchymal transition (EMT) has been well stablished; however, the role as immediate-early regulators is still unclear. Here, we identified a mouse miRNA-host gene lncRNA (lnc-Nr6a1) early upregulated during EMT. We show that this lncRNA is processed giving rise to abundant polyadenylated isoforms, lnc-Nr6a1 and lnc-Nr6a1-2, and a longer non-polyadenylated microprocessor-driven lnc-pri-miRNAS containing clustered pre-miRNA-181a2 and pre-miRNA-181b2 hairpins. Ectopic expression of lnc-Nr6a1-1/2 isoforms enhance cell migration and invasive capacity of the cells, whereas the expression of isoforms and miR-181a2/b2 confers anoikis resistance. Lnc-Nr6a1 gene deletion results in cells with lower adhesion capacity and reduced glycolytic metabolism which are restored by lnc-Nr6a1-1 isoform expression. We perform identification of direct RNA interacting proteins (iDRIP) to identify proteins interacting directly with lnc-Nr6a1-1 isoform. We define a network of interacting proteins, including glycolytic enzymes, desmosome proteins and chaperone proteins and we demonstrated that lnc-Nr6a1-1 isoform directly binds and acts as a scaffold molecule for the assembly of ENO1, ALDOA, GAPDH, PKM glycolytic enzymes along with LDHA, supporting substrate canneling for efficient glycolysis. Our results unveil a role of lnc-Nr6a1 as a multifunctional lncRNA acting as a backbone for multiprotein complexes formation and as a primary microRNAs reservoir.
2022-10-04 | GSE207916 | GEO
Project description:Long noncoding RNAs (lncRNAs) have emerged as key regulators in a wide range of biological processes. The involvement of lncRNAs in epithelial-to-mesenchymal transition (EMT) has been well stablished; however, the role as immediate-early regulators is still unclear. Here, we identified a mouse miRNA-host gene lncRNA (lnc-Nr6a1) early upregulated during EMT. We show that this lncRNA is processed giving rise to abundant polyadenylated isoforms, lnc-Nr6a1 and lnc-Nr6a1-2, and a longer non-polyadenylated microprocessor-driven lnc-pri-miRNAS containing clustered pre-miRNA-181a2 and pre-miRNA-181b2 hairpins. Ectopic expression of lnc-Nr6a1-1/2 isoforms enhance cell migration and invasive capacity of the cells, whereas the expression of isoforms and miR-181a2/b2 confers anoikis resistance. Lnc-Nr6a1 gene deletion results in cells with lower adhesion capacity and reduced glycolytic metabolism which are restored by lnc-Nr6a1-1 isoform expression. We perform identification of direct RNA interacting proteins (iDRIP) to identify proteins interacting directly with lnc-Nr6a1-1 isoform. We define a network of interacting proteins, including glycolytic enzymes, desmosome proteins and chaperone proteins and we demonstrated that lnc-Nr6a1-1 isoform directly binds and acts as a scaffold molecule for the assembly of ENO1, ALDOA, GAPDH, PKM glycolytic enzymes along with LDHA, supporting substrate canneling for efficient glycolysis. Our results unveil a role of lnc-Nr6a1 as a multifunctional lncRNA acting as a backbone for multiprotein complexes formation and as a primary microRNAs reservoir.
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Project description:TGF-beta-upregulated Lnc-Nr6a1 acts as a reservoir of miR-181 and mediates assembly of a glycolytic complex
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Project description:TGF-beta-upregulated Lnc-Nr6a1 acts as a reservoir of miR-181 and mediates assembly of a glycolytic complex [ChIP-seq]
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Project description:Long non-coding RNAs (lncRNAs) have emerged as key regulators in a wide range of biological processes. Here, we identified a mouse miRNA-host gene lncRNA (lnc-Nr6a1) upregulated early during epithelial-to-mesenchymal transition (EMT). We show that when lncRNA is processed, it gives rise to two abundant polyadenylated isoforms, lnc-Nr6a1-1 and lnc-Nr6a1-2, and a longer non-polyadenylated microprocessor-driven lnc-pri-miRNA containing clustered pre-miR-181a2 and pre-miR-181b2 hairpins. Ectopic expression of the lnc-Nr6a1-1 or lnc-Nr6a1-2 isoform enhanced cell migration and the invasive capacity of the cells, whereas the expression of the isoforms and miR-181a2 and miR-181b2 conferred anoikis resistance. Lnc-Nr6a1 gene deletion resulted in cells with lower adhesion capacity and reduced glycolytic metabolism, which are restored by lnc-Nr6a1-1 isoform expression. We performed identification of direct RNA interacting proteins (iDRIP) to identify proteins interacting directly with the lnc-Nr6a1-1 isoform. We defined a network of interacting proteins, including glycolytic enzymes, desmosome proteins and chaperone proteins; and we demonstrated that the lnc-Nr6a1-1 isoform directly binds and acts as a scaffold molecule for the assembly of ENO1, ALDOA, GAPDH, and PKM glycolytic enzymes, along with LDHA, supporting substrate channeling for efficient glycolysis. Our results unveil a role of Lnc-Nr6a1 as a multifunctional lncRNA acting as a backbone for multiprotein complex formation and primary microRNAs.
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