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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: PRJNA523830 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8610570_1.fastq.gz	Fastqsanger.gz
	SRR8610570_2.fastq.gz	Fastqsanger.gz
	SRR8610580_1.fastq.gz	Fastqsanger.gz
	SRR8610580_2.fastq.gz	Fastqsanger.gz
	SRR8610571_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

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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.

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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.

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Long noncoding RNA HITT coordinates with RGS2 to inhibit PD-L1 translation in T cell immunity-proteome

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2022-12-28 | PXD039107 |

Assessment Of Long Noncoding RNA CCAT1 In Colorectal Cancer Patients

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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

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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

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