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P53 activates the long noncoding RNA Pvt1b to inhibit Myc and suppress tumorigenesis

ABSTRACT: p53 activates the long noncoding RNA Pvt1b to inhibit Myc and suppress tumorigenesis

PROVIDER: PRJNA598241 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10807007_1.fastq.gz	Fastqsanger.gz
	SRR10807007_2.fastq.gz	Fastqsanger.gz
	SRR10807008_1.fastq.gz	Fastqsanger.gz
	SRR10807008_2.fastq.gz	Fastqsanger.gz
	SRR10807009_1.fastq.gz	Fastqsanger.gz

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p53 activates the long noncoding RNA Pvt1b to inhibit Myc and suppress tumorigenesis

Project description:p53 activates the long noncoding RNA Pvt1b to inhibit Myc and suppress tumorigenesis

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p53 activates the long noncoding RNA Pvt1b to inhibit Myc and suppress tumorigenesis

Project description:p53 activates the long noncoding RNA Pvt1b to inhibit Myc and suppress tumorigenesis

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p53 activates the long noncoding RNA Pvt1b to inhibit Myc and suppress tumorigenesis

Project description:The tumor suppressor p53 transcriptionally activates target genes to suppress cellular proliferation during stress. p53 has also been implicated in the repression of the proto-oncogene Myc, but the mechanism has remained unclear. Here, we identify Pvt1b, a p53-dependent isoform of the long noncoding RNA (lncRNA) Pvt1, expressed 50 Kb downstream of Myc, which becomes induced by DNA damage or oncogenic signaling and accumulates near its site of transcription. We show that production of the Pvt1b RNA is necessary and sufficient to suppress Myc transcription in cis without altering the chromatin organization of the locus. Inhibition of Pvt1b increases Myc levels and transcriptional activity and promotes cellular proliferation. Furthermore, Pvt1b loss accelerates tumor growth, but not tumor progression, in an autochthonous mouse model of lung cancer. These findings demonstrate that Pvt1b acts at the intersection of the p53 and Myc transcriptional networks to reinforce the anti-proliferative activities of p53.

2020-01-20 | GSE142772 | GEO

p53 Activates the Long Noncoding RNA Pvt1b to Inhibit Myc and Suppress Tumorigenesis.

Project description:The tumor suppressor p53 transcriptionally activates target genes to suppress cellular proliferation during stress. p53 has also been implicated in the repression of the proto-oncogene Myc, but the mechanism has remained unclear. Here, we identify Pvt1b, a p53-dependent isoform of the long noncoding RNA (lncRNA) Pvt1, expressed 50 kb downstream of Myc, which becomes induced by DNA damage or oncogenic signaling and accumulates near its site of transcription. We show that production of the Pvt1b RNA is necessary and sufficient to suppress Myc transcription in cis without altering the chromatin organization of the locus. Inhibition of Pvt1b increases Myc levels and transcriptional activity and promotes cellular proliferation. Furthermore, Pvt1b loss accelerates tumor growth, but not tumor progression, in an autochthonous mouse model of lung cancer. These findings demonstrate that Pvt1b acts at the intersection of the p53 and Myc transcriptional networks to reinforce the anti-proliferative activities of p53.

| S-EPMC7184554 | biostudies-literature

p53 activates the long noncoding RNA Pvt1b to inhibit Myc and suppress tumorigenesis

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

2020-01-20 | GSE143204 | GEO

p53 activates the long noncoding RNA Pvt1b to inhibit Myc and suppress tumorigenesis

Project description:P53 activation in response to cellular stress has long been known to result in downregulation of c-myc, a gene that is frequently overexpressed in cancer due to its role in promoting cellular proliferation. However, the mechanism underlying this p53 dependent myc repression is poorly understood. Here we report p53 regulation of the lncRNA PVT1, a neighboring myc gene which is upregulated following p53 activation via p53 binding to a canonical p53 response element (p53RE) in the first intron of PVT1. Specifically, we find that p53 activation results in induction of an isoform of PVT1 initiated from an alternative first exon, which we have termed PVT1alt. When the PVT1 p53RE is mutated and PVT1alt induction is inhibited, we observe increased levels of myc mRNA in cells undergoing DNA damage or oncogenic stress and corresponding increases in cellular proliferation. The PVT1alt RNA is required for this p53-dependent myc repression, suggesting a important growth suppressive role for this lncRNA in the p53 response. Our study reveals a novel mode of myc regulation in cis by an alternative lncRNA isoform, providing insight into an important mechanism of crosstalk between the p53 and myc transcriptional networks.

2020-01-20 | GSE126940 | GEO

MEX3A mediates p53 degradation to suppress ferroptosis and facilitate ovarian cancer tumorigenesis

Project description:MEX3A mediates p53 degradation to suppress ferroptosis and facilitate ovarian cancer tumorigenesis

| PRJNA824850 | ENA

FANCD2 Activates Transcription of TAp63 and Suppresses Tumorigenesis

Project description:Fanconi Anemia (FA) is a rare genetic disorder characterized by an increased susceptibility to squamous cell cancers. Fifteen FA genes are known, and the encoded proteins cooperate in a common DNA repair pathway. A critical step is the monoubiquitination of the FANCD2 protein, and cells from most FA patients are deficient in this step. How monoubiquitinated FANCD2 suppresses squamous cell cancers is unknown. Here we show that Fancd2-deficient mice are prone to Ras oncogene-driven skin carcinogenesis, while Usp1-deficient mice, expressing elevated cellular levels of Fancd2-Ub, are resistant to skin tumors. Moreover, Fancd2-Ub activates the transcription of the tumor suppressor TAp63, thereby promoting cellular senescence and blocking skin tumorigenesis. For FA patients, the reduction of FANCD2-Ub and TAp63 protein levels may account for their susceptibility to squamous cell neoplasia. Taken together, Usp1 inhibition may be a useful strategy for upregulating TAp63 and preventing or treating squamous cell cancers in the general non-FA population. Examination of FANCD2 binding after UV treatment in 293T cells

2013-06-27 | E-GEOD-46902 | biostudies-arrayexpress

MEX3A mediates p53 degradation to suppress ferroptosis and facilitate ovarian cancer tumorigenesis

Project description:Epithelial ovarian cancer (OC) is a highly heterogeneous and malignant female cancer with an overall low survival rate. p53 mutation is a predominant genetic factor thought to be responsible for poor clinical outcome. Despite the fact that ovarian clear cell carcinoma (OCCC) shows more severe prognosis, drug resistance, metastasis and recurrence compared to other OC subtypes, mutations in p53 are much less frequent. The underlying mechanisms crucial for tumorigenesis and malignancy of OC harboring wild-type (WT) p53 remain poorly understood. We found that upregulation of MEX3A, which is a dual-function protein containing a RING finger domain and an RNA binding domain, was correlated with poor survival in OC. MEX3A overexpression enhanced tumorigenic activity in RMG-1 and OVISE OCCC cell lines. In contrast, depletion of MEX3A in PA-1 ovarian teratocarcinoma cells and TOV21G OCCC cells reduced cell survival and proliferative ability in cell-based assays, as well as inhibited tumor growth and prolonged survival in orthotopic xenograft models. MEX3A depletion did not alter p53 mRNA level but did increase the protein stability of WT p53. MEX3A-mediated p53 protein degradation was crucial to prevent ferroptosis and enhance tumorigenesis as p53 knockdown reversed the effects of MEX3A depletion. Together, our observations identified MEX3A as an important oncogenic factor promoting tumorigenesis in OC cells harboring WT p53.

2022-10-25 | GSE200509 | GEO

SnoN activates p53 directly to regulate aging and tumorigenesis.

Project description:We have identified SnoN as a direct activator of p53 to accelerate aging and inhibit tumorigenesis. SnoN has been shown previously to promote proliferation and transformation by antagonizing TGF? signaling. We show that elimination of this TGF? antagonistic activity of SnoN in vivo results in accelerated aging and resistance to tumorigenesis. The SnoN knockin mice display a shortened lifespan, decreased reproductivity, osteoporosis, reduced regenerative capacity, and other aging phenotypes, similar to that found in mice expressing an active p53. These activities of SnoN rely on the ability of SnoN to activate p53. SnoN can bind directly to p53 and compete with Mdm2 for binding to p53, preventing p53 ubiquitination and degradation and additionally facilitating p53 acetylation and phosphorylation. SnoN also binds to p53 on the promoter of p53 responsive genes to promote transcription activation. This activation of p53 by SnoN is necessary for its antitumorigenic and progeria activities in vivo because elimination of one copy of p53 reverses the aging phenotypes and accelerates tumorigenesis. Thus, we have revealed a novel function of SnoN in regulating aging and tumorigenesis by directly activating p53.

| S-EPMC3897278 | biostudies-literature

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