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TGFβ1-Induced EMT in the MCF10A Mammary Epithelial Cell Line Model Is Executed Independently of SNAIL1 and ZEB1 but Relies on JUNB-Coordinated Transcriptional Regulation

ABSTRACT: TGFβ1-Induced EMT in the MCF10A Mammary Epithelial Cell Line Model Is Executed Independently of SNAIL1 and ZEB1 but Relies on JUNB-Coordinated Transcriptional Regulation

PROVIDER: PRJNA865784 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20814348_1.fastq.gz	Fastqsanger.gz
	SRR20814348_2.fastq.gz	Fastqsanger.gz
	SRR20814349_1.fastq.gz	Fastqsanger.gz
	SRR20814349_2.fastq.gz	Fastqsanger.gz
	SRR20814350_1.fastq.gz	Fastqsanger.gz

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TGFβ1-Induced EMT in the MCF10A Mammary Epithelial Cell Line Model Is Executed Independently of SNAIL1 and ZEB1 but Relies on JUNB-Coordinated Transcriptional Regulation

Project description:Epithelial-mesenchymal transition (EMT) fosters cancer cell invasion and metastasis, the main cause of cancer-related mortality. Growing evidence that SNAIL and ZEB transcription factors, typically portrayed as master regulators of EMT, may be dispensable for this process, led us to re-investigate its mechanistic underpinnings. For this, we used an unbiased computational ap-proach that integrated time-resolved analyses of chromatin structure and differential gene ex-pression, to predict transcriptional regulators of TGFβ1-inducible EMT in the MCF10A mam-mary epithelial cell line model. Bioinformatic analyses indicated comparatively minor contri-butions of SNAIL proteins and ZEB1 to TGFβ1-induced EMT, whereas the AP-1 subunit JUNB was anticipated to have a much larger impact. CRISPR/Cas9-mediated loss-of-function studies confirmed that TGFβ1-induced EMT proceeded independently of SNAIL proteins and ZEB1. In contrast, JUNB was necessary and sufficient for EMT in MCF10A cells, but not in A549 lung can-cer cells, indicating cell-type-specificity of JUNB EMT-regulatory capacity. Nonetheless, the JUNB-dependence of EMT-associated transcriptional reprogramming in MCF10A cells allowed to define a gene expression signature which was regulated by TGFβ1 in diverse cellular back-grounds, showed positively correlated expression with TGFβ signaling in multiple cancer tran-scriptomes, and was predictive of patient survival in several cancer types. Altogether, our find-ings provide novel mechanistic insights into the context-dependent control of TGFβ1-driven EMT and thereby may lead to improved diagnostic and therapeutic options.

2023-01-17 | GSE210498 | GEO

TGFβ1-Induced EMT in the MCF10A Mammary Epithelial Cell Line Model Is Executed Independently of SNAIL1 and ZEB1 but Relies on JUNB-Coordinated Transcriptional Regulation

2023-01-17 | GSE210499 | GEO

TGFβ1-Induced EMT in the MCF10A Mammary Epithelial Cell Line Model Is Executed Independently of SNAIL1 and ZEB1 but Relies on JUNB-Coordinated Transcriptional Regulation

2023-01-17 | GSE210496 | GEO

TGFβ1-Induced EMT in the MCF10A Mammary Epithelial Cell Line Model Is Executed Independently of SNAIL1 and ZEB1 but Relies on JUNB-Coordinated Transcriptional Regulation

Project description:TGFβ1-Induced EMT in the MCF10A Mammary Epithelial Cell Line Model Is Executed Independently of SNAIL1 and ZEB1 but Relies on JUNB-Coordinated Transcriptional Regulation

| PRJNA865786 | ENA

TGFβ1-Induced EMT in the MCF10A Mammary Epithelial Cell Line Model Is Executed Independently of SNAIL1 and ZEB1 but Relies on JUNB-Coordinated Transcriptional Regulation

Project description:TGFβ1-Induced EMT in the MCF10A Mammary Epithelial Cell Line Model Is Executed Independently of SNAIL1 and ZEB1 but Relies on JUNB-Coordinated Transcriptional Regulation

| PRJNA865785 | ENA

TGFβ1-Induced EMT in the MCF10A Mammary Epithelial Cell Line Model Is Executed Independently of SNAIL1 and ZEB1 but Relies on JUNB-Coordinated Transcriptional Regulation.

Project description:Epithelial-mesenchymal transition (EMT) fosters cancer cell invasion and metastasis, the main cause of cancer-related mortality. Growing evidence that SNAIL and ZEB transcription factors, typically portrayed as master regulators of EMT, may be dispensable for this process, led us to re-investigate its mechanistic underpinnings. For this, we used an unbiased computational approach that integrated time-resolved analyses of chromatin structure and differential gene expression, to predict transcriptional regulators of TGFβ1-inducible EMT in the MCF10A mammary epithelial cell line model. Bioinformatic analyses indicated comparatively minor contributions of SNAIL proteins and ZEB1 to TGFβ1-induced EMT, whereas the AP-1 subunit JUNB was anticipated to have a much larger impact. CRISPR/Cas9-mediated loss-of-function studies confirmed that TGFβ1-induced EMT proceeded independently of SNAIL proteins and ZEB1. In contrast, JUNB was necessary and sufficient for EMT in MCF10A cells, but not in A549 lung cancer cells, indicating cell-type-specificity of JUNB EMT-regulatory capacity. Nonetheless, the JUNB-dependence of EMT-associated transcriptional reprogramming in MCF10A cells allowed to define a gene expression signature which was regulated by TGFβ1 in diverse cellular backgrounds, showed positively correlated expression with TGFβ signaling in multiple cancer transcriptomes, and was predictive of patient survival in several cancer types. Altogether, our findings provide novel mechanistic insights into the context-dependent control of TGFβ1-driven EMT and thereby may lead to improved diagnostic and therapeutic options.

| S-EPMC9856774 | biostudies-literature

TGFβ1 promotes collective invasion of oncogenically transformed intestinal organoids by inducing partial epithelial-mesenchymal transition independently of Snail1 and Zeb1

Project description:Cancer cells simultaneously featuring epithelial and mesenchymal traits appear particularly competent to invade and metastasize. However, genetic prerequisites and signaling pathways promoting such partial epithelial-to-mesenchymal transitions (EMT) remain obscure. Here we report that murine intestinal organoids with hyperactive Wnt and MAPK signaling, and mutant Trp53 are purely epithelial and non-invasive in vitro, but initiate a collective invasion program when treated with TGFβ1. Invasive organoids reciprocally interact with the extracellular matrix (ECM), and autonomously deposit and remodel components thereof. Although cells at the organoid/ECM interface shed certain epithelial characteristics, invasive organoids largely maintain epithelial gene expression while concomitantly upregulating a mesenchymal program. TGFβ1-induced phenotypic changes involve canonical, Smad4-dependent signaling, yet, are unimpeded by knockout of Snai1 and Zeb1 - otherwise key regulators of epithelial-to-mesenchymal transitions. The finding of TGFβ1-inducible, Snail1/Zeb1-independent collective invasion of oncogenically transformed intestinal organoids provides novel mechanistic insights and broadens the spectrum of context-dependent manifestations of partial EMT.

2022-01-24 | GSE156553 | GEO

Zeb1 and Snail1 engage miR-200f transcriptional and epigenetic regulation during EMT

Project description:Cell plasticity is emerging as a key regulator of tumor progression and metastasis. During carcinoma dissemination epithelial cells undergo epithelial to mesenchymal transition (EMT) processes characterized by the acquisition of migratory/invasive properties, while the reverse, mesenchymal to epithelial transition (MET) process, is also essential for metastasis outgrowth. Different transcription factors, called EMT-TFs, including Snail, bHLH and Zeb families are drivers of the EMT branch of epithelial plasticity, and can be post-transcriptionally downregulated by several miRNAs, as the miR-200 family. The specific or redundant role of different EMT-TFs and their functional interrelations are not fully understood. To study the interplay between different EMT-TFs, comprehensive gain and loss-of-function studies of Snail1, Snail2 and/or Zeb1 factors were performed in the prototypical MDCK cell model system. We here describe that Snail1 and Zeb1 are mutually required for EMT induction while continuous Snail1 and Snail2 expression, but not Zeb1, is needed for maintenance of the mesenchymal phenotype in MDCK cells. In this model system, EMT is coordinated by Snail1 and Zeb1 through transcriptional and epigenetic downregulation of the miR-200 family. Interestingly, Snail1 is involved in epigenetic CpG DNA methylation of the miR-200 loci, essential to maintain the mesenchymal phenotype. The present results thus define a novel functional interplay between Snail and Zeb EMT-TFs in miR200f regulation providing a molecular link to their previous involvement in the generation of EMT process in vivo. Expression analysis of MDCK over-expression EMT-TF Analysis of 7 overexpression MDCK cells each of them using biological rpelicates (MDCK-E47, Snail2, Snail1, Twist1, Tiwst2, Zeb1, Zeb2)

2014-09-09 | E-GEOD-61217 | biostudies-arrayexpress

Zeb1 and Snail1 engage miR-200f transcriptional and epigenetic regulation during EMT

2014-09-09 | GSE61217 | GEO

TGFβ1 promotes collective invasion of oncogenically transformed intestinal organoids by inducing partial epithelial-mesenchymal transition independently of Snail1 and Zeb1

Project description:TGFβ1 promotes collective invasion of oncogenically transformed intestinal organoids by inducing partial epithelial-mesenchymal transition independently of Snail1 and Zeb1

| PRJNA658333 | ENA

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