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LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (RIP-Seq)

ABSTRACT: LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (RIP-Seq)

PROVIDER: PRJNA760307 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15711607_1.fastq.gz	Fastqsanger.gz
	SRR15711607_2.fastq.gz	Fastqsanger.gz
	SRR15711608_1.fastq.gz	Fastqsanger.gz
	SRR15711608_2.fastq.gz	Fastqsanger.gz
	SRR15711609_1.fastq.gz	Fastqsanger.gz

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LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (RIP-Seq)

Project description:High expression of LIN28B is associated with aggressive malignancy and poor survival. Here, probing MYCN-amplified neuroblastoma as a model system, we show that LIN28B expression is associated with enhanced cell migration in vitro and invasive and metastatic behavior in murine xenografts. Sequence analysis of the polyribosome fraction of LIN28B-expressing neuroblastoma cells revealed let-7 independent enrichment of transcripts encoding components of the translational and ribosomal apparatus, particularly those with higher adenine/uridine (AU)-content, and depletion of transcripts of neuronal developmental programs. We further show that LIN28B utilizes both its cold shock and zinc finger RNA binding domains to preferentially interact with MYCN-induced transcripts of the ribosomal complex, enhancing their translation. These data demonstrate that LIN28B couples the MYCN-driven transcriptional program to enhanced ribosomal translation, thereby implicating LIN28B as a post-transcriptional driver of the metastatic phenotype.

2022-09-30 | GSE183336 | GEO

LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (RNA-Seq)

Project description:High expression of LIN28B is associated with aggressive malignancy and poor survival. Here, probing MYCN-amplified neuroblastoma as a model system, we show that LIN28B expression is associated with enhanced cell migration in vitro and invasive and metastatic behavior in murine xenografts. Sequence analysis of the polyribosome fraction of LIN28B-expressing neuroblastoma cells revealed let-7 independent enrichment of transcripts encoding components of the translational and ribosomal apparatus, particularly those with higher Adenine/Uridine (AU)-content, and depletion of GC-rich transcripts of neuronal developmental programs. We further show that LIN28B utilizes both its cold shock and zinc finger RNA binding domains to preferentially interact with MYCN-induced transcripts of the ribosomal complex, enhancing their translation. These data demonstrate that LIN28B couples the MYCN-driven transcriptional program to enhanced ribosomal translation, thereby implicating LIN28B as a post-transcriptional driver of the metastatic phenotype.

2022-09-30 | GSE158320 | GEO

LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (Polysome sequencing)

2022-09-30 | GSE183335 | GEO

LIN28B alters ribosomal dynamics to promote metastasis in MYCN induced malignancy

Project description:LIN28B alters ribosomal dynamics to promote metastasis in MYCN induced malignancy

| PRJNA760326 | ENA

LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (RNA-Seq)

Project description:LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (RNA-Seq)

| PRJNA664805 | ENA

LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (Polysome sequencing)

Project description:LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (Polysome sequencing)

| PRJNA760306 | ENA

LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy.

Project description:High expression of LIN28B is associated with aggressive malignancy and poor survival. Here, probing MYCN-amplified neuroblastoma as a model system, we showed that LIN28B expression was associated with enhanced cell migration in vitro and invasive and metastatic behavior in murine xenografts. Sequence analysis of the polyribosome fraction of LIN28B-expressing neuroblastoma cells revealed let-7-independent enrichment of transcripts encoding components of the translational and ribosomal apparatus and depletion of transcripts of neuronal developmental programs. We further observed that LIN28B utilizes both its cold shock and zinc finger RNA binding domains to preferentially interact with MYCN-induced transcripts of the ribosomal complex, enhancing their translation. These data demonstrated that LIN28B couples the MYCN-driven transcriptional program to enhanced ribosomal translation, thereby implicating LIN28B as a posttranscriptional driver of the metastatic phenotype.

| S-EPMC8592552 | biostudies-literature

LIN28B Regulates Transcription and Potentiates MYCN-induced Neuroblastoma in a let-7-independent Manner [ChIP-seq]

Project description:LIN28B is highly expressed in neuroblastoma and promotes tumorigenesis at least in part through inhibition of let-7 microRNA biogenesis. Here, we report that overexpression of either wild-type LIN28B, or a LIN28B mutant that is unable to bind and inhibit let-7, accelerates the onset and increases the penetrance of MYCN-induced neuroblastoma, potentiates the invasion and migration of transformed sympathetic neuroblasts and drives the distant metastases in vivo. Genome-wide ChIP-seq analysis and co-immunoprecipitation experiments show that LIN28B indirectly binds active gene promoters in neuroblastoma cells through an interaction with ZNF143 and activates the expression of downstream targets, including GSK3B and L1CAM, which are involved in neuronal cell adhesion and migration. These findings reveal an unexpected, let-7-independent function for LIN28B in transcriptional regulation during neuroblastoma pathogenesis.

2020-07-22 | GSE138742 | GEO

LIN28B Regulates Transcription and Potentiates MYCN-induced Neuroblastoma in a let-7-independent Manner [RNA-seq]

2020-07-22 | GSE138741 | GEO

LIN28B alters ribosomal dynamics to promote metastasis in MYCN induced malignancy

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

2022-09-30 | GSE183351 | GEO