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Integrated multi-omics analysis of RB-loss identifies widespread cellular programming and synthetic weaknesses.

ABSTRACT: Integrated multi-omics analysis of RB-loss identifies widespread cellular programming and synthetic weaknesses.

PROVIDER: PRJNA589550 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10446391_1.fastq.gz	Fastqsanger.gz
	SRR10446391_2.fastq.gz	Fastqsanger.gz
	SRR10446392_1.fastq.gz	Fastqsanger.gz
	SRR10446392_2.fastq.gz	Fastqsanger.gz
	SRR10446393_1.fastq.gz	Fastqsanger.gz

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Integrated multi-omics analysis of RB-loss identifies widespread cellular programming and synthetic weaknesses.

Project description:To assess how cells adapt to RB-loss, we quantitatively measured transcriptional, changes in diploid non-tumorigenic human cells transiently depleted of RB.

2021-02-15 | GSE140383 | GEO

Integrated multi-omics analysis of RB-loss identifies widespread cellular programming and synthetic weaknesses.

Project description:Inactivation of RB is one of the hallmarks of cancer, however gaps remain in our understanding of how RB-loss changes human cells. Here we show that pRB-depletion results in cellular reprogramming, we quantitatively measured how RB-depletion altered the transcriptional, proteomic and metabolic output of non-tumorigenic RPE1 human cells. These profiles identified widespread changes in metabolic and cell stress response factors previously linked to E2F function. In addition, we find a number of additional pathways that are sensitive to RB-depletion that are not E2F-regulated that may represent compensatory mechanisms to support the growth of RB-depleted cells. To determine whether these molecular changes are also present in RB1-/- tumors, we compared these results to Retinoblastoma and Small Cell Lung Cancer data, and identified widespread conservation of alterations found in RPE1 cells. To define which of these changes contribute to the growth of cells with de-regulated E2F activity, we assayed how inhibiting or depleting these proteins affected the growth of RB1-/- cells and of Drosophila E2f1-RNAi models in vivo. From this analysis, we identify key metabolic pathways that are essential for the growth of pRB-deleted human cells.

| S-EPMC8371045 | biostudies-literature

Integrated multi-omics analysis of RB-loss identifies widespread cellular programming and synthetic weaknesses

Project description:Multiplexed proteomics using TMT10 and the SPS-MS3 method on an Orbitrap Fusion mass spectrometer has been used to study the loss of retinoblastoma 1, RB, in human cell lines. Samples were measured in three TMT pools (TMT1, TMT2, TMT3). Each pool was fractionated by basic pH reversed-phase liquid chromatography (bRPLC) and per pool twelve fractions were analyzed by mass spectrometry. A bridge channel from combined digests of all samples was used to enable a combined analysis of the data from the three TMT pools. The RAW files are: Miles_RB_TMT1_fraction01 to 12 Miles_RB_TMT2_fraction01 to 12 Miles_RB_TMT3_fraction01 to 12 The TMT labeling of the samples was as follows: FF-DOX (TMT1, 127n), FF+DOX (TMT1, 127c), RB25-DOX (TMT1, 128n), RB25-DOX (TMT1, 128c), RB25+DOX (TMT1, 130c), RB25+DOX (TMT2, 127n), RB26-DOX (TMT2, 129c), RB26-DOX ((TMT2, 130n), RB26+DOX (TMT3, 128n), RB26+DOX (TMT3, 128c). The bridge channel was at 126 for all three TMT pools.

2019-12-26 | MSV000084736 | MassIVE

Synthetic lethality between Rb, p53 and miR-17~92 in retinal progenitors suppresses retinoblastoma formation_murine data

Project description:Although Dicer1 functions as a haploinsufficient tumour suppressor its complete loss of function is selected against during tumourigenesis. Here we show that homozygous loss of Dicer1 prevents retinoblastoma formation in mice by synthetic lethality with combined inactivation of the p53 and Rb tumor suppressor pathways. We show that Dicer1 deficiency is tolerated in Rb-deficient retinal progenitor cells harbouring an intact p53 pathway, but not in absence of p53. The synthetic lethal interaction is mediated by the oncogenic miR-17?92 cluster since its deletion phenocopies Dicer1 loss in this context. Accordingly, miR-17?92- inactivation suppresses retinoblastoma formation in mice and co-silencing of miR17/20a and p53 cooperatively decrease the viability of pre-formed human retinoblastoma cells. These data provide important insights into what underlies selective pressure against loss of Dicer1 during tumorigenesis and indicate that targeting Dicer or miR-17-20a family members should be explored as a potential selective therapeutic approach for retinoblastoma prevention and/or treatment. 23 murine samples

2012-07-05 | E-GEOD-39106 | biostudies-arrayexpress

Synthetic lethality between Rb, p53 and miR-17~92 in retinal progenitors suppresses retinoblastoma formation_human data

Project description:Although Dicer1 functions as a haploinsufficient tumour suppressor its complete loss of function is selected against during tumourigenesis. Here we show that homozygous loss of Dicer1 prevents retinoblastoma formation in mice by synthetic lethality with combined inactivation of the p53 and Rb tumor suppressor pathways. We show that Dicer1 deficiency is tolerated in Rb-deficient retinal progenitor cells harbouring an intact p53 pathway, but not in absence of p53. The synthetic lethal interaction is mediated by the oncogenic miR-17∼92 cluster since its deletion phenocopies Dicer1 loss in this context. Accordingly, miR-17∼92- inactivation suppresses retinoblastoma formation in mice and co-silencing of miR17/20a and p53 cooperatively decrease the viability of pre-formed human retinoblastoma cells. These data provide important insights into what underlies selective pressure against loss of Dicer1 during tumorigenesis and indicate that targeting Dicer or miR-17-20a family members should be explored as a potential selective therapeutic approach for retinoblastoma prevention and/or treatment. 36 human samples

2012-07-05 | E-GEOD-39105 | biostudies-arrayexpress

Synthetic lethality between Rb, p53 and miR-17~92 in retinal progenitors suppresses retinoblastoma formation_murine data

Project description:Although Dicer1 functions as a haploinsufficient tumour suppressor its complete loss of function is selected against during tumourigenesis. Here we show that homozygous loss of Dicer1 prevents retinoblastoma formation in mice by synthetic lethality with combined inactivation of the p53 and Rb tumor suppressor pathways. We show that Dicer1 deficiency is tolerated in Rb-deficient retinal progenitor cells harbouring an intact p53 pathway, but not in absence of p53. The synthetic lethal interaction is mediated by the oncogenic miR-17∼92 cluster since its deletion phenocopies Dicer1 loss in this context. Accordingly, miR-17∼92- inactivation suppresses retinoblastoma formation in mice and co-silencing of miR17/20a and p53 cooperatively decrease the viability of pre-formed human retinoblastoma cells. These data provide important insights into what underlies selective pressure against loss of Dicer1 during tumorigenesis and indicate that targeting Dicer or miR-17-20a family members should be explored as a potential selective therapeutic approach for retinoblastoma prevention and/or treatment.

2012-07-05 | GSE39106 | GEO

Synthetic lethality between Rb, p53 and miR-17~92 in retinal progenitors suppresses retinoblastoma formation_human data

Project description:Although Dicer1 functions as a haploinsufficient tumour suppressor its complete loss of function is selected against during tumourigenesis. Here we show that homozygous loss of Dicer1 prevents retinoblastoma formation in mice by synthetic lethality with combined inactivation of the p53 and Rb tumor suppressor pathways. We show that Dicer1 deficiency is tolerated in Rb-deficient retinal progenitor cells harbouring an intact p53 pathway, but not in absence of p53. The synthetic lethal interaction is mediated by the oncogenic miR-17∼92 cluster since its deletion phenocopies Dicer1 loss in this context. Accordingly, miR-17∼92- inactivation suppresses retinoblastoma formation in mice and co-silencing of miR17/20a and p53 cooperatively decrease the viability of pre-formed human retinoblastoma cells. These data provide important insights into what underlies selective pressure against loss of Dicer1 during tumorigenesis and indicate that targeting Dicer or miR-17-20a family members should be explored as a potential selective therapeutic approach for retinoblastoma prevention and/or treatment.

2012-07-05 | GSE39105 | GEO

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