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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)

| PRJNA450316 | ENA

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)

| PRJNA450394 | ENA

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.

2020-08-27 | GSE113179 | GEO

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

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

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

RBM25 is a global splicing factor promoting inclusion of alternatively spliced exons

Project description:The goal of this study was to determine the role of RBM25 in pre-mRNA splicing and examine whether lysine 77 contributes to this function.

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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

Identification of Rbm25-binding RNAs in bone-marrow-derived macrophages by RIP-seq

Project description:To identify the potential mRNAs that bound by Rbm25, which might be the direct target of Rbm25 for alternative splicing in murine macrophages.

2024-11-06 | GSE240159 | GEO

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