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Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis

ABSTRACT: Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis

PROVIDER: PRJNA324117 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1134680.fastq.gz	Fastqsanger.gz
	SRR1134681.fastq.gz	Fastqsanger.gz
	SRR1134682.fastq.gz	Fastqsanger.gz
	SRR1134676.fastq.gz	Fastqsanger.gz
	SRR1134677.fastq.gz	Fastqsanger.gz

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Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis.

Project description:Prep1 is a tumor-suppressor, whereas Meis1 is an oncogene. We show that to perform these activities in MEFs both proteins competitively hetero-dimerize with Pbx1. Meis1 alone transforms Prep1-deficient fibroblasts while Prep1 overexpression inhibits Meis1 tumorigenicity. Pbx1 can therefore alternatively act as oncogene or tumor-suppressor. Prep1 post-translationally controls the level of Meis1 decreasing its stability by sequestering Pbx1. The different levels of Meis1 and the presence of Prep1 are followed at the transcriptional level by the induction of specific transcriptional signatures. The decrease of Meis1 prevents Meis1 interaction with Ddx3x and Ddx5, which are essential for Meis1 tumorigenesis, and modifies the growth promoting DNA binding landscape of Meis1 to the growth controlling landscape of Prep1. Hence the key feature of Prep1 tumor inhibiting activity is the control of Meis1 stability. Examination of Prep1 and Meis1 in three cell type

2014-03-05 | E-GEOD-54221 | biostudies-arrayexpress

Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis [hP]

2016-06-01 | GSE58802 | GEO

Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis [hP]

2016-06-01 | E-GEOD-58802 | biostudies-arrayexpress

Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis [hM, hMP]

2014-03-05 | GSE54221 | GEO

Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis

Project description:Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis

| PRJNA324117 | ENA

Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis.

Project description:Pbx-regulating protein-1 (Prep1) is a tumor suppressor, whereas myeloid ecotropic viral integration site-1 (Meis1) is an oncogene. We show that, to perform these activities in mouse embryonic fibroblasts, both proteins competitively heterodimerize with pre-B-cell leukemia homeobox-1 (Pbx1). Meis1 alone transforms Prep1-deficient fibroblasts, whereas Prep1 overexpression inhibits Meis1 tumorigenicity. Pbx1 can, therefore, alternatively act as an oncogene or tumor suppressor. Prep1 posttranslationally controls the level of Meis1, decreasing its stability by sequestering Pbx1. The different levels of Meis1 and the presence of Prep1 are followed at the transcriptional level by the induction of specific transcriptional signatures. The decrease of Meis1 prevents Meis1 interaction with Ddx3x and Ddx5, which are essential for Meis1 tumorigenesis, and modifies the growth-promoting DNA binding landscape of Meis1 to the growth-controlling landscape of Prep1. Hence, the key feature of Prep1 tumor-inhibiting activity is the control of Meis1 stability.

| S-EPMC3956142 | biostudies-literature

Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-06-01 | E-GEOD-82135 | biostudies-arrayexpress

Prep1 and Meis1 competition for Pbx1 binding regulates protein stability and tumorigenesis

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

2016-06-01 | GSE82135 | GEO

Meis1 induces and Prep1 suppresses tumors by exploiting low affinity AP1 binding sites.

Project description:We have defined the tumor and tumor suppressor signature for Meis1 and Prep1 (pKnox1), respectively, using ChIP-seq and RNA-seq in a cell system in which tumor suppressor Prep1 and oncogene Meis1 compete for tumorigenesis [GSE54221; GSE58802]. In this paper we report that the number of Meis1 or Prep1 DNA binding sites increases linearly with the level of expression of the two transcription factors. Overexpression of Meis1 induces tumors. At the molecular level it modifies the DNA target specificity by increasing the number of low-affinity binding sites, which results in a different choice of consensus sequences with predominance of sites normally bound by the AP1 transcription factor family. Upon concomitant overexpression of Prep1 and Meis1 tumorigenesis is inhibited. Prep1 dominates over Meis1 not only because it partially decreases Meis1 protein level but also because it prevents the binding to a substantial fraction of the low affinity binding sites. Overall, overexpression of Prep1 reverses the nature of the bound and regulated genes from stimulatory to inhibitory of signal transduction and transcription, which suppresses tumorigenesis. By identifying the Meis1 tumor signature, specific relevant signaling pathways are identified. In line with these results, tumorigenic Meis1-overexpressing cells are uniquely hypersensitive to inhibitors of the MAPK/Akt pathways.

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Meis1 induces and Prep1 suppresses tumors by exploiting low affinity AP1 binding sites.

2016-06-25 | E-GEOD-58818 | biostudies-arrayexpress