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EMT-driven plasticity prospectively increases cell-cell variability to promote therapeutic adaptation in breast cancer

ABSTRACT: EMT-driven plasticity prospectively increases cell-cell variability to promote therapeutic adaptation in breast cancer

PROVIDER: PRJNA1098856 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR28622003.fastq.gz	Fastqsanger.gz
	SRR28622004.fastq.gz	Fastqsanger.gz
	SRR28622005.fastq.gz	Fastqsanger.gz
	SRR28622006.fastq.gz	Fastqsanger.gz

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EMT-driven plasticity prospectively increases cell-cell variability to promote therapeutic adaptation in breast cancer.

Project description:Cellular plasticity enables cancer cells to adapt non-genetically, thereby preventing therapeutic success. The epithelial-mesenchymal transition (EMT) is a type of plasticity linked to resistance and metastasis. However, its exact impact on population diversity and its dynamics under chemotherapy is unknown. We used single-cell transcriptomics to investigate phenotypic diversity dynamics upon treatment in two in vitro models of triple negative breast cancer (TNBC), where EMT-driven plasticity is either induced or spontaneously occurring. We report that EMT-driven plasticity confers higher phenotypic cell-cell variability (p < 0.001) while enriching for stem-like cells. Genetic and phenotypic cell-cell variability were not consistently correlated. High-plasticity populations displayed more pre-adapted cells before treatment (p = 0.03). In a population displaying spontaneous EMT and phenotypic variation, pre-adapted cells were a rare minority of high-scoring outliers whose expression patterns correlated with survival in TNBC patients subjected to chemotherapy (p = 0.03). Higher plasticity was not associated with a partial EMT status. Our results provide novel insights on how EMT-driven plasticity promotes a prospective diversification process increasing population phenotypic diversity, which can yield rare pre-adapted states before treatment. This highlights the need to tackle phenotypic diversity prior to treatment in high-plasticity tumours.

| S-EPMC11789407 | biostudies-literature

EMT-driven plasticity prospectively increases cell-cell variability to promote therapeutic adaptation in breast cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-12-04 | GSE263731 | GEO

FGF4 stimulation increases variability in mESCs [scRNA-seq]

Project description:FGF4 stimulation increases variability in mESCs [scRNA-seq]

| PRJNA1077953 | ENA

FGF4 stimulation increases variability in mESCs [scRNA-seq]

Project description:FGF4 is essential for Epiblast and Primitive Endoderm formation in the mouse embryo and promotes differentiation of mouse embryonic stem cells. However, different FGF-concentrations regulate gene expression quantitatively remained an open question. We used single-cell RNA sequencing to quantify transcriptional variability and dynamics upon FGF4 stimulation of Fgf4-mutant mESCs.

2025-02-26 | GSE256059 | GEO

Identification of chromatin accessibility domains in EMT and breast cancer stem cell formation.

Project description:Epithelial-mesenchymal transition (EMT), the process whereby cells gain migratory and invasive properties characteristic of mesenchymal cells, plays a central role in embryogenesis and wound healing in a wide range of tissues. However, EMT has also been linked to the formation of cancer stem cells (CSCs). Many of the signaling pathways involved in EMT have also been implicated in CSC formation but the processes that contribute uniquely to CSC formation remain elusive. We have previously demonstrated that PKCÎ¸ activation is critical for EMT induction and concomitant CSC formation in the breast cancer luminal epithelial cell line, MCF7. To discover how PKC-induced alterations in the epigenome influence the EMT and CSC formation in MCF-7 cells, we employed a combination of expression profiling and Formaldehyde Assisted Regulatory Elements (FAIRE)-sequencing in order to reveal novel links between gene expression and DNA accessibility changes after PKCÎ¸ activation. We found that, during EMT, increases in accessibility generally occurred in regions away from transcription start sites, low in CpG, enriched with chromatin marks of enhancer elements and motifs for FOX, AP1, TEAD and AP2. Increases in FOX and AP-1 motif accessibility were associated with genes that exhibited increased expression in CSC, while increased AP-2 accessibility was associated with genes that had higher expression in non-CSCs. This study revealed novel regions of DNA accessibility induced by PKC that contribute to the understanding of how epigenomic plasticity of cells undergoing EMT leads to the activation of genes that drive the CSC program. 2 biological samples were analysed with 2 biological replicates each and a mixed total input.

2016-03-10 | E-GEOD-71023 | biostudies-arrayexpress

Identifying molecular mechanisms of neural crest (NC) EMT and cell migration

Project description:Purpose: To identify differntially expressed transcripts in TP-0903 treated embryos that impair cranila NC EMT and cell migration in zebrafish embryos Methods: zebrafish embryos treated at 13 hpf with 5-7uM TP-0903 and DMSO for 1-, 4- and 8-hrs at 28Â°C. 35 embryos were collected for each treatment. Results: TP-0903 increases expression of several retinoic acid target genes including genes from within the retinoid pathway Conclusions: TP-0903 causes a direct increase in RA signaling that impairs cranial NC EMT and cell migration in zebrafihs embryos mRNA profiles of zebrafish embryos treated with TP-0903 and DMSO were generated by RNA-Seq, in quadruplicates, using Illumina Hi Seq

2016-02-18 | E-GEOD-72322 | biostudies-arrayexpress

Investigating delayed-onset Drug Hypersensitivity Reactions Prospectively

Project description:Investigating delayed-onset Drug Hypersensitivity Reactions Prospectively

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Investigating delayed-onset Drug Hypersensitivity Reactions Prospectively

Project description:Investigating delayed-onset Drug Hypersensitivity Reactions Prospectively

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A cancer avatar models prospectively guides therapy

Project description:A cancer avatar models prospectively guides therapy

| PRJNA475104 | ENA

The EMT-activator Zeb1 is crucial for cellular plasticity and drives metastasis in pancreatic cancer

Project description:Depletion of Zeb1 in a KPC-model for pancreatic cancer affected strongly the formation of precursor lesions, tumour grading, invasion and notably metastasis during PDAC progression. In this context, EMT is important for metastasis, but there is variability and specificity (and not redundancy) in the role and function of different EMT-inducing transcription factors.

2017-03-16 | GSE87472 | GEO

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