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Predicting master transcription factors from pan-cancer expression data

ABSTRACT: Predicting master transcription factors from pan-cancer expression data

PROVIDER: PRJNA640799 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12060400.fastq.gz	Fastqsanger.gz
	SRR12060401.fastq.gz	Fastqsanger.gz
	SRR12060402.fastq.gz	Fastqsanger.gz
	SRR12060403.fastq.gz	Fastqsanger.gz
	SRR12060404.fastq.gz	Fastqsanger.gz

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Predicting Master Transcription Factors from Pan-Cancer Expression Data

Project description:Predicting Master Transcription Factors from Pan-Cancer Expression Data

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Predicting Master Transcription Factors from Pan-Cancer Expression Data

Project description:Critical developmental “master transcription factors” (MTFs) can be subverted during tumorigenesis to control expression of oncogenic transcriptional programs. Current approaches to identify MTFs rely on chromatin immunoprecipitation-sequencing data, which is currently unavailable for many cancer types. We developed the CaCTS (Cancer Core Transcription factor Specificity) algorithm to prioritize candidate MTFs using pan-cancer RNA-sequencing data. CaCTS identified candidate MTFs across 34 tumor types and 140 subtypes, including known MTFs. We also made novel predictions, including for cancer types/subtypes for which MTFs are unknown. This included PAX8, SOX17, and MECOM as candidate MTFs in ovarian cancer (OV). In OV cells, these factors are required for viability, lie proximal to super-enhancers, co-occupy regulatory elements globally and co-bind at critical gene loci encoding OV biomarkers. Identification of tumor MTFs, especially for tumor types with limited understanding of transcriptional drivers, paves the way to therapeutic targeting of MTFs in a broad spectrum of cancers.

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Predicting master transcription factors from pan-cancer expression data

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Predicting master transcription factors from pan-cancer expression data.

Project description:Critical developmental “master transcription factors” (MTFs) can be subverted during tumorigenesis to control oncogenic transcriptional programs. Current approaches to identifying MTFs rely on ChIP-seq data, which is unavailable for many cancers. We developed the CaCTS (Cancer Core Transcription factor Specificity) algorithm to prioritize candidate MTFs using pan-cancer RNA sequencing data. CaCTS identified candidate MTFs across 34 tumor types and 140 subtypes including predictions for cancer types/subtypes for which MTFs are unknown, including e.g. PAX8, SOX17, and MECOM as candidates in ovarian cancer (OvCa). In OvCa cells, consistent with known MTF properties, these factors are required for viability, lie proximal to superenhancers, co-occupy regulatory elements globally, co-bind loci encoding OvCa biomarkers, and are sensitive to pharmacologic inhibition of transcription. Our predictions of MTFs, especially for tumor types with limited understanding of transcriptional drivers, pave the way to therapeutic targeting of MTFs in a broad spectrum of cancers.

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Master transcription factors in corneal epithelial cells

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Pan-cancer predictions of transcription factors mediating aberrant DNA methylation

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SMAD2/3 potentiate cell identity conversions with master transcription factors

Project description:The exogenous expression of master transcription factors (TFs) is a powerful and exciting approach to convert cellular identity. Yet, the generation of desired cell types is often plagued by inefficiency, slow kinetics and inability to produce mature cell types. Through investigations of the molecular mechanisms of induced plurpipotent stem cell generation, we discovered that expression of constitutively active Smad2/3 (Smad2CA/3CA), together with the Yamanaka factors, could dramatically improve the efficiency and kinetics of reprogramming. Mechanistically, SMAD3 interacted with both co-activators and reprogramming factors, bridging their interaction during reprogramming. Fascinatingly, SMAD2/3 interact with a multitude of master TFs in different cell types, and conversions of B cells to macrophages, myoblasts to adipocytes, and human fibroblasts to neurons were also markedly enhanced when their master TFs were co-expressed with Smad3CA. These results revealed the existence of shared molecular mechanisms underlying diverse TF-mediated cellular conversions, and demonstrated SMAD2/3 as a widely applicable booster.

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IRF2BP2 affects T-ALL cell proliferation by cooperating with master transcription factors

Project description:IRF2BP2 affects T-ALL cell proliferation by cooperating with master transcription factors

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Master Transcription Factors and Mediator Establish Super-Enhancers at Key Cell Identity Genes [gene expression]

Project description:The master transcription factors Oct4, Sox2 and Nanog bind enhancer elements and recruit the Mediator co-activator to activate much of the gene expression program of embryonic stem cells (ESCs). We report here that the ESC master transcription factors and Mediator form “super-enhancers” at most genes known to control the pluripotent state, including those encoding the master transcription factors themselves. These super-enhancers consist of extraordinarily large genomic domains occupied by exceptional amounts of Oct4, Sox2, Nanog, Klf4, Esrrb and Mediator. Super-enhancers stimulate considerably higher transcription than typical enhancers in vivo and in reporter vectors. Reduced levels of Oct4 or Mediator cause preferential loss of expression of super-enhancer-associated genes relative to other genes, suggesting how changes in gene expression programs might be accomplished during development. In other more differentiated cells, super-enhancers containing cell-type-specific master transcription factors are also found at genes that define cell identity. These results implicate super-enhancers in the control of mammalian cell identity and differentiation.

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