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Dysregulation of p53-RBM25-mediated circAMOTL1L biogenesis contributes to prostate cancer progression

ABSTRACT: Dysregulation of p53-RBM25-mediated circAMOTL1L biogenesis contributes to prostate cancer progression

PROVIDER: PRJNA450385 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7009362_1.fastq.gz	Fastqsanger.gz
	SRR7009362_2.fastq.gz	Fastqsanger.gz
	SRR7009363_1.fastq.gz	Fastqsanger.gz
	SRR7009363_2.fastq.gz	Fastqsanger.gz
	SRR7009364_1.fastq.gz	Fastqsanger.gz

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Dysregulation of p53-RBM25-mediated circAMOTL1L biogenesis contributes to prostate cancer progression (Agilent circRNA data set)

Project description:Dysregulation of p53-RBM25-mediated circAMOTL1L biogenesis contributes to prostate cancer progression (Agilent circRNA data set)

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Dysregulation of p53-RBM25-mediated circAMOTL1L biogenesis contributes to prostate cancer progression (RNA-seq data set)

Project description:Dysregulation of p53-RBM25-mediated circAMOTL1L biogenesis contributes to prostate cancer progression (RNA-seq data set)

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Dysregulation of p53-RBM25-mediated circAMOTL1L biogenesis contributes to prostate cancer progression (RNA-seq data set)

Project description:To clarify the effect of p53 on RBP gene expression, we knocked out p53 gene in PC3 cells to generate p53 knockout stable cell line (p53-/- PC3 cells) and examined the expression of the known RBP genes by RNA sequencing.

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Dysregulation of p53-RBM25-mediated circAMOTL1L biogenesis contributes to prostate cancer progression

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

2020-08-27 | GSE113180 | GEO

p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [expression]

Project description:The role of ribosome biogenesis in erythroid development is supported by the recognition of erythroid defects in ribosomopathies in both Diamond-Blackfan anemia and 5q- syndrome. Whether ribosome biogenesis exerts a regulatory function on normal erythroid development is still unknown. In the present study, a detailed characterization of ribosome biogenesis dynamics during human and murine erythropoiesis shows that ribosome biogenesis is abruptly interrupted by the drop of rDNA transcription and the collapse of ribosomal protein neo-synthesis. Its premature arrest by RNA polI inhibitor, CX-5461 targets the proliferation of immature erythroblasts. We also show that p53 is activated spontaneously or in response to CX-5461 concomitantly to ribosome biogenesis arrest, and drives a transcriptional program in which genes involved in cell cycle arrest, negative regulation of apoptosis and DNA damage response were upregulated. RNA polI transcriptional stress results in nucleolar disruption and activation of ATR-CHK1-p53 pathway. Our results imply that the timing of ribosome biogenesis extinction and p53 activation are crucial for erythroid development. In ribosomopathies in which ribosome availability is altered by unbalanced production of ribosomal proteins, the threshold of ribosome biogenesis down-regulation could be prematurely reached and together with pathological p53 activation prevents a normal expansion of erythroid progenitors.

2020-09-14 | GSE137951 | GEO

p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [ChIP-Seq]

2020-09-14 | GSE157208 | GEO

Dysregulation of p53-RBM25-mediated circAMOTL1L biogenesis contributes to prostate cancer progression through the circAMOTL1L-miR-193a-5p-Pcdha pathway.

Project description:p53, circRNAs and miRNAs are important components of the regulatory network that activates the EMT program in cancer metastasis. In prostate cancer (PCa), however, it has not been investigated whether and how p53 regulates EMT by circRNAs and miRNAs. Here we show that a Amotl1-derived circRNA, termed circAMOTL1L, is downregulated in human PCa, and that decreased circAMOTL1L facilitates PCa cell migration and invasion through downregulating E-cadherin and upregulating vimentin, thus leading to EMT and PCa progression. Mechanistically, we demonstrate that circAMOTL1L serves as a sponge for binding miR-193a-5p in PCa cells, relieving miR-193a-5p repression of Pcdha gene cluster (a subset of the cadherin superfamily members). Accordingly, dysregulation of the circAMOTL1L-miR-193a-5p-Pcdha8 regulatory pathway mediated by circAMOTL1L downregulation contributes to PCa growth in vivo. Further, we show that RBM25 binds directly to circAMOTL1L and induces its biogenesis, whereas p53 regulates EMT via direct activation of RBM25 gene. These findings have linked p53/RBM25-mediated circAMOTL1L-miR-193a-5p-Pcdha regulatory axis to EMT in metastatic progression of PCa. Targeting this newly identified regulatory axis provides a potential therapeutic strategy for aggressive PCa.

| S-EPMC6484770 | biostudies-literature

p53 activation during ribosome biogenesis regulates normal erythroid differentiation.

Project description:p53 activation during ribosome biogenesis regulates normal erythroid differentiation.

| PRJNA660448 | ENA

Dysregulation of p53-RBM25-mediated circAMOTL1L biogenesis contributes to prostate cancer progression (Agilent circRNA data set)

Project description:To explore the molecular mechanisms underlying circRNA role in prostate carcinogenesis and progression of PCa, we first used circular RNA microarrays to acquire circRNA profiles in PCa tissues. Five pairs of samples were taken from the two different areas, i.e., high-grade PCa (Gleason>8) and low-grade PCa (Gleason< 6), within the same PCa sample

2020-08-27 | GSE113153 | GEO

RNA exosome mutations in pontocerebellar hypoplasia alter ribosome biogenesis and p53 levels

Project description:The eukaryotic RNA exosome is a ubiquitously expressed complex of nine core proteins (EXOSC1-9) and associated nucleases responsible for RNA processing and degradation. Autosomal recessive mutations in EXOSC3, EXOSC8, EXOSC9 and the exosome cofactor RBM7 cause pontocerebellar hypoplasia and motor neuronopathy. To understand the importance of the exosome in neurodegeneration, we investigated the consequences of exosome mutations on RNA metabolism and cellular survival in zebrafish and human cell models. We observed that levels of mRNAs encoding p53 and ribosome biogenesis factors are upregulated in zebrafish lines with homozygous mutations of exosc8 or exosc9, respectively. In addition, exosome deficiency leads to increased levels of multiple non-coding RNAs (e.g. tRNAs, snoRNAs, scaRNAs). Consistent with higher p53 levels, mutant zebrafish have a reduced head size, smaller brain and cerebellum caused by an increased number of apoptotic cells during development. Downregulation of EXOSC9 in human cells leads to p53 protein stabilisation and G2/M cell cycle arrest. The work provides explanation for the pathogenesis of exosome-related disorders and highlights the link between exosome function, ribosome biogenesis and p53-dependent signalling.

2020-05-30 | GSE151452 | GEO

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