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An mRNA processing pathway suppresses metastasis by governing translational control from the nucleus [Ribo-seq, RNA-seq]

ABSTRACT: An mRNA processing pathway suppresses metastasis by governing translational control from the nucleus [Ribo-seq, RNA-seq]

PROVIDER: PRJNA898352 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22192973.fastq.gz	Fastqsanger.gz
	SRR22192974.fastq.gz	Fastqsanger.gz
	SRR22192975.fastq.gz	Fastqsanger.gz
	SRR22192976.fastq.gz	Fastqsanger.gz
	SRR22192977.fastq.gz	Fastqsanger.gz

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An mRNA processing pathway suppresses metastasis by governing translational control from the nucleus [Ribo-seq, RNA-seq]

Project description:Cancer cells often co-opt post-transcriptional regulatory mechanisms to achieve pathologic expression of gene networks that drive metastasis. Translational control is a major regulatory hub in oncogenesis, however its effects on cancer progression remain poorly understood. To address this, we used ribosome profiling to compare genome-wide translation efficiencies of poorly and highly metastatic breast cancer cells and patient-derived xenografts. We developed novel regression-based methods to analyze ribosome profiling and alternative polyadenylation data, and identified HNRNPC as a translational controller of a specific mRNA regulon. Mechanistically, HNRNPC, in concert with PABPC4, binds near to poly(A) signals, thereby governing the alternative polyadenylation of a set of mRNAs. We found that HNRNPC and PABPC4 are downregulated in highly metastatic cells, which causes HNRNPC-bound mRNAs to undergo 3’ UTR lengthening and subsequently, translational repression. We showed that modulating HNRNPC expression impacts the metastatic capacity of breast cancer cells in xenograft mouse models. We also found that a small molecule, previously shown to induce a distal-to-proximal poly(A) site switching, counteracts the HNRNPC-PABPC4 driven deregulation of alternative polyadenylation and decreases the metastatic lung colonization by breast cancer cells in vivo.

2023-02-20 | GSE217287 | GEO

An mRNA processing pathway suppresses metastasis by governing translational control from the nucleus [Quant-seq]

Project description:An mRNA processing pathway suppresses metastasis by governing translational control from the nucleus [Quant-seq]

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An mRNA processing pathway suppresses metastasis by governing translational control from the nucleus [Quant-seq]

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IGHMBP2 deletion suppresses translation and activates the integrated stress response [Ribo-Seq]

Project description:IGHMBP2 is a non-essential, superfamily 1 DNA/RNA helicase with incompletely understood biological function. Mutagenesis in IGHMBP2 is found in patients with rare neuromuscular diseases SMARD1 and CMT2S. IGHMBP2 is implicated in translational and transcriptional regulation via biochemical association with ribosomal proteins, pre-rRNA processing factors, and tRNA-related species. To uncover the cellular consequences of perturbing IGHMBP2, we generated full and partial IGHMBP2 deletion K562 cell lines. We performed Ribo-seq and RNA-seq and identified diverse gene expression changes due to IGHMBP2 deletion, including ATF4 upregulation.

2023-12-19 | GSE248888 | GEO

Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing [Ribo-seq]

Project description:Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing [Ribo-seq]

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An mRNA processing pathway suppresses metastasis by governing translational control from the nucleus.

Project description:Cancer cells often co-opt post-transcriptional regulatory mechanisms to achieve pathologic expression of gene networks that drive metastasis. Translational control is a major regulatory hub in oncogenesis; however, its effects on cancer progression remain poorly understood. Here, to address this, we used ribosome profiling to compare genome-wide translation efficiencies of poorly and highly metastatic breast cancer cells and patient-derived xenografts. We developed dedicated regression-based methods to analyse ribosome profiling and alternative polyadenylation data, and identified heterogeneous nuclear ribonucleoprotein C (HNRNPC) as a translational controller of a specific mRNA regulon. We found that HNRNPC is downregulated in highly metastatic cells, which causes HNRNPC-bound mRNAs to undergo 3' untranslated region lengthening and, subsequently, translational repression. We showed that modulating HNRNPC expression impacts the metastatic capacity of breast cancer cells in xenograft mouse models. In addition, the reduced expression of HNRNPC and its regulon is associated with the worse prognosis in breast cancer patient cohorts.

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The translational landscape of phenylephrine-treated neonatal rat cardiomyocytes [Ribo-seq]

Project description:The translational landscape of phenylephrine-treated neonatal rat cardiomyocytes [Ribo-seq]

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DUX4 orchestrates translational reprograming by broadly suppressing translation efficiency [Ribo-seq]

Project description:DUX4 orchestrates translational reprograming by broadly suppressing translation efficiency [Ribo-seq]

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Ultrasensitive Ribo-seq reveals translational landscapes during mammalian oocyte-to-embryo transition and pre-implantation development

Project description:In mammals, translational control plays critical roles during oocyte-to-embryo transition (OET) when transcription ceases. However, the underlying regulatory mechanisms remain challenging to study. Here, using low-input Ribo-seq (Ribo-lite), we investigated translational landscapes during OET using 30-150 mouse oocytes or embryos per stage. Ribo-lite can also accommodate single oocytes. Combining PAIso-seq to interrogate poly(A) tail lengths, we found a global switch of translatome that closely parallels changes of poly(A) tails upon meiotic resumption. Translation activation correlates with polyadenylation and is supported by polyadenylation signal proximal cytoplasmic polyadenylation elements (papCPEs) in 3' untranslated regions. By contrast, translation repression parallels global de-adenylation. The latter includes transcripts containing no CPEs or non-papCPEs, which encode many transcription regulators that are preferentially re-activated before zygotic genome activation. CCR4-NOT, the major de-adenylation complex, and its key adaptor protein BTG4 regulate translation downregulation often independent of RNA decay. BTG4 is not essential for global de-adenylation but is required for selective gene de-adenylation and production of very short-tailed transcripts. In sum, our data reveal intimate interplays among translation, RNA stability and poly(A) tail length regulation underlying mammalian OET. Note: RNA-seq data for PN5 zygotes, early two-cell, late two-cell, four-cell and eight-cell stages and ICM were obtained from our previous publication (Zhang et al., Nature, 2016: Allelic reprogramming of the histone modification H3K4me3 in early mammalian development, GSE71434).

2022-04-19 | GSE165782 | GEO

Heterogeneous ribonucleoprotein interactions and impeded translational elongation in the respiratory tissue of SARS-CoV-2 pathology (Ribo-Seq)

Project description:Translational regulation in in vivo tissue environments during viral pathogenesis has hardly been scrutinized due to the lack of tissue translatomes upon viral infection despite a number of the translatome studies on virus-infected cells cultured in vitro. We constructed the first temporal profile of lung translatomes during SARS-CoV-2 pathogenesis by applying ribosome profiling (Ribo-seq) to a severe COVID-19 mouse model. Unexpectedly, we observed gradual accumulations of non-canonical Ribo-seq reads representing hitherto-unidentified ribonucleoproteins (RNPs) that are likely involved in impeded translational elongation in the infected tissues. Contemporarily developing ribosome heterogeneity with prominently deviated 5S rRNP association supported the malfunction of elongating ribosomes. The analyses of canonical Riboseq reads (ribosome footprints) highlighted two obstructive characteristics to host gene expression: attenuated translation for transcriptionally up-regulated genes including immune response genes and ribosome stalling on codons within transmembrane domain-coding regions. Our study elucidates hidden molecular features of gene regulation in vivo underlying SARS-CoV-2 pathogenesis.

2023-12-01 | GSE222249 | GEO

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