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Murine Prostate Tissue: Rb1 null vs. Rb1 E2F binding deficient mutant

ABSTRACT: Transcriptional profilling of 60 day old prostate tissue from Rb1F/F:Trp53F/F:PB-Cre4 or Rb1R654W/F:Trp53F/F:PB-cre4 mice versus wild type prostate tissue. Profiles used to compare deregulation of known E2F target genes in prostate tissue expressing a mutant Rb1 gene to tissue lacking Rb1 expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE25615 | GEO | 2010/11/27

SECONDARY ACCESSION(S): PRJNA133957

REPOSITORIES: GEO

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Murine Prostate Tissue: Rb1 null vs. Rb1 E2F binding deficient mutant

Project description:Transcriptional profilling of 60 day old prostate tissue from Rb1F/F:Trp53F/F:PB-Cre4 or Rb1R654W/F:Trp53F/F:PB-cre4 mice versus wild type prostate tissue. Profiles used to compare deregulation of known E2F target genes in prostate tissue expressing a mutant Rb1 gene to tissue lacking Rb1 expression. Tissue from two Rb1F/F:Trp53F/F:PB-Cre4 (null) mice or two Rb1654/F:Trp53F/F:PB-cre4 (mutant) mice compared to a pool of tissue from 3 wild type mice using two color arrays.

2010-11-27 | E-GEOD-25615 | biostudies-arrayexpress

RB1 loss promotes a noncanonical activator function of LSD1 and sensitizes castration-resistant prostate cancer to LSD1 inhibition [ChIP-seq]

Project description:Genomic loss of RB1 is a common alteration in castration-resistant prostate cancer (CRPC) and is associated with poor patient outcomes. RB1-loss is also a driver event that promotes the neuroendocrine transdifferentiation of prostate cancer (PCa). The loss of Rb protein disrupts the Rb-E2F repressor complex and thus hyperactivates E2F transcription activators. While the impact of RB1-loss on PCa progression and linage plasticity has been previously studied, the underline mechanisms remain unclear. Using an integrated cistromic and transcriptomic analysis, we have characterized Rb activities in multiple CRPC models by identifying Rb directly regulated genes and revealed that Rb has distinct binding sites and targets in TP53-mutated CRPC. Significantly, we show that RB1-loss promotes the noncanonical activator function of LSD1/KDM1A, which stabilizes chromatin binding of E2F1, and hence sensitizes CRPC tumor to the LSD1 inhibitor treatment. These results provide new molecular insights of Rb activity in PCa progression and suggest LSD1 as a potential therapeutic target in CRPC with RB1-loss.

2022-01-14 | GSE176402 | GEO

RB1 loss promotes a noncanonical activator function of LSD1 and sensitizes castration-resistant prostate cancer to LSD1 inhibition [RNA-seq]

2022-01-14 | GSE176403 | GEO

Mus musculus

Project description:Murine Prostate Tissue: Rb1 null vs. Rb1 E2F binding deficient mutant

| PRJNA133957 | ENA

A retinoblastoma allele that is mutated at its common E2F interaction site inhibits cell proliferation in gene targeted mice

Project description:The retinoblastoma protein (pRB) is best known for regulating cell proliferation through E2F transcription factors. In this report we investigate the properties of a targeted mutation that disrupts pRB interactions with the transactivation domain of E2Fs. Mice that carry this mutation endogenously (Rb1∆G) are defective in regulating E2F target genes. Surprisingly, cell cycle regulation in Rb1∆G/∆G MEFs strongly resembles that of wild type. In a serum deprivation induced cell cycle exit, Rb1∆G/∆G MEFs display a similar magnitude of E2F target gene derepression as Rb1-/-, even though Rb1∆G/∆G cells exit the cell cycle normally. Interestingly, cell cycle arrest in Rb1∆G/∆G MEFs is responsive to p16 expression, indicating that the ΔG-pRB protein can be activated in G1 to arrest proliferation through non-E2F mechanisms. Some Rb1∆G/∆G mice die neonatally with a muscle degeneration phenotype, while the others live a normal lifespan with no evidence of spontaneous tumor formation. Histological analysis reveals discrete examples of hyperplasia in the mammary epithelium, but most tissues appear normal while being accompanied by derepression of pRB regulated E2F targets. This suggests that non-E2F, pRB dependent pathways may have a more relevant role in proliferative control than previously identified.

2014-04-14 | GSE54924 | GEO

RNA sequencing of wildtype, PTEN single knockout (SKO), and PTEN;Rb1 double knockout (DKO) mouse prostate organoids

Project description:The goal of this study was to perform transcriptomics on wildtype, PTEN single knockout (SKO) and PTEN;Rb1 double knockout (DKO) mouse prostate organoids. We isolated basal cells from PTEN floxed and PTEN;Rb1 floxed mouse prostates and infected with either RFP control or Cre recombinase to establish wildtype, SKO, and DKO mouse prostate organoids.

2023-09-01 | GSE221020 | GEO

MMTV-Myc tumor development in E2F-null backgrounds

Project description:Advances in genomic signatures have begun to dissect breast cancer heterogeneity, and application of these signatures will allow the prediction of which pathways are important in tumor development. Here we used genomic signatures to predict involvement of specific E2F transcription factors in Myc-induced tumors. We genetically tested this prediction by interbreeding Myc transgenics with mice lacking various activator E2F alleles. Tumor latency decreased in the E2F1 mutant background and significantly increased in both the E2F2 and E2F3 mutants. Investigating the mechanism behind these changes revealed a reduction in apoptosis in the E2F1 knockout strain. E2F2 and E2F3 mutant backgrounds alleviated Myc effects on the mammary gland, reducing the susceptible tumor target population. Gene expression data from tumors revealed that the E2F2 knockout background resulted in fewer tumors with EMT, corresponding with a reduction in probability of Ras activation. In human breast cancer we found that a low probability of E2F2 pathway activation was associated with increased relapse-free survival time. Together these data illustrate the predictive utility of genomic signatures in deciphering the heterogeneity within breast cancer and illustrate the unique genetic requirements for individual E2Fs in mediating tumorigenesis in both mouse models and human breast cancer. MMTV-Myc tumors were generated in an E2F wild-type, E2F1 null, E2F2 null and E2F3 heterozygous background. When the primary tumor reached the endpoint, the tumors were flash frozen. 20 tumors from each genotype were selected for microarray analysis.

2011-12-29 | E-GEOD-24594 | biostudies-arrayexpress

RNA sequencing of BRCA2 and/or RB1 knockout LNCaP cells

Project description:Human prostate cancer LNCaP cells infected with Lentivirus carried huamn BRCA2 gRNA alone or in combination with lentivirus carrying human RB1 shRNA. Infected cell were selcted by drug selection and the knockdown were confirm by westernblot or qPCR

2020-05-07 | GSE114153 | GEO

MMTV-Myc tumor development in E2F-null backgrounds

2011-12-29 | GSE24594 | GEO

RNA sequencing of PTEN,Rb1 double knockout (DKO) mouse prostate organoids treated with vehicle or the small molecule mitochondrial pyruvate carrier (MPC) inhibitor UK5099

Project description:The goal of this study was to determine how pharmacological inhibition of the mitochondrial pyruvate carrier (MPC) alters lineage identity in transformed prostate organoids. We isolated basal cells from PTEN,Rb1 floxed mouse prostates and infected with Cre recombinase to establish PTEN, Rb1 double knockout (DKO) mouse prostate organoids. We then treated the DKO organoids with vehicle or 10uM UK5099 for five days.

2023-09-01 | GSE221021 | GEO

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