Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Comparison of the RB loss-induced E2F1 cistrome in hormone-therapy sensitive and castration-resistant prostate cancer [ChIP-seq]

ABSTRACT: These studies examine the consequence of RB loss on E2F1 function across prostate cancer progression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE154191 | GEO | 2021/04/26

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Investigation of the AR cistrome in response to RB depletion in castration-resistant prostate cancer

Project description:These studies examine the consequence of RB loss on AR function in late stage disease

2022-04-01 | GSE171511 | GEO

Comparison of the RB loss-induced E2F1 cistrome in hormone-therapy sensitive and castration-resistant prostate cancer [ChIP-seq]

Project description:Comparison of the RB loss-induced E2F1 cistrome in hormone-therapy sensitive and castration-resistant prostate cancer [ChIP-seq]

| PRJNA645395 | ENA

Comparison of the RB loss-induced transcrptiome in hormone-therapy sensitive and castration-resistant prostate cancer [RNA-seq]

Project description:These studies examine the biological networks altered after RB loss across prostate cancer progression.

2021-04-26 | GSE154190 | GEO

E2F1 loss induces spontaneous tumour development in Rb-deficient epidermis

Project description:The specific ablation of Rb1 gene in epidermis (RbF/F;K14cre) promotes proliferation and altered differentiation but does not produce spontaneous tumour development. These phenotypic changes are associated with increased expression of E2F members and E2F-dependent transcriptional activity. Here, we have focused on the possible dependence on E2F1 gene function. We have generated mice that lack Rb1 in epidermis in an inducible manner (RbF/F;K14creERTM). These mice are indistinguishable from those lacking pRb in this tissue in a constitutive manner (RbF/F;K14cre). In an E2F1-null background (RbF/F;K14creERTM; E2F1-/- mice), the phenotype due to acute Rb1 loss is not ameliorated by E2F1 loss, but rather exacerbated, indicating that pRb functions in epidermis do not rely solely on E2F1. On the other hand, RbF/F;K14creERTM;E2F1-/- mice develope spontaneous epidermal tumours of hair follicle origin with high incidence. These tumours, which retain a functional p19arf/p53 axis, also show aberrant activation of βcatenin/Wnt pathway. Gene expression studies revealed that these tumours display relevant similarities with specific human tumours. These data demonstrate that the Rb/E2F1 axis exerts essential functions not only in maintaining epidermal homeostasis, but also in suppressing tumour development in epidermis, and that the disruption of this pathway may induce tumour progression through specific alteration of developmental programs. Gene expression was compared between normal mouse skin, skin from transgenic RbF/F;K14creERTM; E2F1-/- , E2F1-/-, and RbF/F;K14creERTM; E2F1-/- mouse, and carcinomas arising in the skin of RbF/F;K14creERTM; E2F1-/- mouse. All mice were treated with tamoxifen.

2012-08-20 | E-GEOD-38048 | biostudies-arrayexpress

Identification of the RB loss-induced transcriptome and E2F1 cistrome in prostate cancer

Project description:Identification of the RB loss-induced transcriptome and E2F1 cistrome in prostate cancer

| PRJNA374914 | ENA

Identification of the RB loss-induced E2F1 cistrome in prostate cancer [ChIP-seq]

Project description:The retinoblastoma protein (RB) is preferentially lost in the progression to castrate resistant prostate cancer (CRPC). However, the alterations associated with such loss have been scantly described. The current study aims to provide molecular mechanisms underlying Rb loss-driven CRPC phenotypes.

2018-02-22 | GSE94958 | GEO

E2F1 loss induces spontaneous tumour development in Rb-deficient epidermis

2012-08-20 | GSE38048 | GEO

RNA-seq Analysis of Castration-Resistant Prostate Cancer With Knock-down of E2F1

Project description:From castration resistant prostate cancer (CRPC) regulatory network, we found over 90% negative feedback loop went through E2F1. And we detected PC3 and DU145 cells with depletion of E2F1 through the invasion, migration, proliferation and apoptosis experiments. In order to identify which genes trigger these phenomenon and regulatory mechanism of E2F1 in CRPC, we performed the gene expression between the vector and under the knockdown of E2F1 in PC3 and DU145 cells by RNA sequencing (RNA-seq). To investigate differentially expressed genes (false discovery rate (FDR) <0.05, |log2 (Fold Change)| > 1) between vector control and shE2F1 of CRPC cells, we performed processing RNA-Seq data using the Basespace. Then we verified some common two cells’ differentially expressed genes through quantitative real-time PCR.

2019-10-18 | GSE121258 | GEO

p21 Regulates Wnt-Notch Balance via DREAM/MMB/Rb-E2F1 and Maintains Intestinal Stem Cell Homeostasis

Project description:The crosstalk and balance regulation of Wnt-Notch have been known to be essential for cell fate decision and tissue regeneration, while how the balance is maintained and how the Wnt-Notch pathways are connected with the cell cycle regulation are still not clear. In the mouse model with accelerated aging phenotypes due to the loss of cell cycle inhibitor p21 function in Werner syndrome background, we observed the imbalance of Wnt-Notch signaling, along with the fast turnover of intestinal epithelia, which might cause the abnormal mobilization of stem cells, exhaust the stem cell reservoir, and result in the accelerated aging phenotypes. We revealed that the loss of p21 caused the shift of DREAM/Rb complex to MMB/E2F1 complex and the fast turnover of intestinal epithelia. Importantly, we identified the E2F1 as the transcriptional regulator for Notch1, which connected the p21-DREAM/MMB/Rb-E2F1 pathway with Wnt-Notch pathway. The overexpression of p21 rescued the imbalance of Wnt-Notch pathway. Our data identify p21 as an important factor in maintaining sequential mobilization, proliferation, and homeostasis of intestinal stem cells.

2023-12-10 | GSE248188 | GEO

EZH2 enables germinal center formation through epigenetic silencing of CDKN1A and an Rb-E2F1 positive feedback loop

Project description:The EZH2 histone methyltransferase is required for B cells to form germinal centers (GCs). Here we show that EZH2 mediates GC formation through repression of cyclin-dependent kinase inhibitor CDKN1A (p21Cip1). Deletion of Cdkn1a rescued the GC reaction in Ezh2 knockout mice. To study the effects of EZH2 in primary GC B cells we generated and validated a 3D B cell follicular organoid system that mimics the endogenous GC reaction. Using this system we found that depletion of EZH2 suppressed G1 to S phase transition of GC B cells in a Cdkn1a dependent manner. GC B cells of Cdkn1a;Ezh2 double knockout mice exhibited high levels of phospho Rb, indicating that loss of Cdkn1a allows progression of cell cycle. Moreover, we show that the transcription factor E2F1 plays a major role in inducing EZH2 upregulation during the GC reaction. E2F1 deficient mice manifest impaired GC responses, which was rescued by restoring EZH2 expression, thus defining a positive feedback loop whereby EZH2 controls GC B cell proliferation by suppressing CDKN1A, allowing cell cycle progression with a concomitant phosphorylation of Rb and release of E2F1.

2017-08-10 | GSE95491 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data