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Phenotypic heterogeneity driven by plasticity of the intermediate EMT state governs disease progression and metastasis in breast cancer

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE172613 | GEO | 2022/02/15

REPOSITORIES: GEO

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Phenotypic heterogeneity driven by plasticity of the intermediate EMT state governs disease progression and metastasis in breast cancer [RNA-seq]

Project description:The Epithelial-to-Mesenchymal Transition (EMT) is a dynamic cellular program that is frequently used by cancer cells to increase migratory and invasive cell characteristics. It is a key contributor to both heterogeneity and chemo-resistance and metastasis in many solid tumors, including triple negative breast cancer. In particular, the intermediate or hybrid EMT state has increased tumor initiating and stem-like properties. Here, we have identified multiple distinct EMT states derived from the human breast cell line, SUM149PT, including three unique intermediate states, possessing distinct migratory, tumor initiating, and metastatic qualities. We have used this model to interrogate the epigenetic landscape of these distinct EMT states in a multi-omics approach, identifying and RUNX2 as relevant in regulating the intermediate state, as well as to develop a novel multiplexed staining approach to evaluate E-M heterogeneity (EMH) and overall EMT score in orthotopic tumors as well as patient tumor samples. This model reveals insights into the complex EMT spectrum of cell states, the networks that control them, and how EMT plasticity contributes to tumor heterogeneity in breast cancer.

2022-02-15 | GSE172609 | GEO

Phenotypic heterogeneity driven by plasticity of the intermediate EMT state governs disease progression and metastasis in breast cancer [ATAC-seq]

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Phenotypic heterogeneity driven by plasticity of the intermediate EMT state governs disease progression and metastasis in breast cancer

Project description:Phenotypic heterogeneity driven by plasticity of the intermediate EMT state governs disease progression and metastasis in breast cancer

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Phenotypic heterogeneity driven by plasticity of the intermediate EMT state governs disease progression and metastasis in breast cancer [ATAC-seq]

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Project description:Phenotypic heterogeneity driven by plasticity of the intermediate EMT state governs disease progression and metastasis in breast cancer [RNA-seq]

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Mechanical confinement governs phenotypic plasticity in melanoma

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

2024-01-24 | GSE253803 | GEO

Mechanical confinement governs phenotypic plasticity in melanoma [HMGB2OE_ATACseq]

Project description:Phenotype switching is a form of cellular plasticity in which cancer cells reversibly move between two opposite extremes - proliferative versus invasive states. While it has long been hypothesised that such switching is triggered by external cues, the identity of these cues has remained elusive. Here, we demonstrate that mechanical confinement mediates phenotype switching through chromatin remodelling. Using a zebrafish model of melanoma coupled with human samples, we profiled tumour cells at the interface between the tumour and surrounding microenvironment. Morphological analysis of these rare cells showed flattened, elliptical nuclei suggestive of mechanical confinement by nearby adjacent tissue. Spatial and single-cell transcriptomics demonstrated that the interface cells adopted a gene program of neuronal invasion, including acquisition of an acetylated tubulin cage that protects the nucleus during migration. We identified the DNA-bending protein HMGB2 as a confinement-induced mediator of the neuronal state. HMGB2 is upregulated in confined cells, and quantitative modelling revealed that confinement prolongs contact time between HMGB2 and chromatin, leading to changes in chromatin configuration that favour the neuronal phenotype. Genetic disruption of HMGB2 showed that it regulates the trade-off between proliferative and invasive states, in which confined HMGB2high tumour cells are less proliferative but more drug resistant. Our results implicate the mechanical microenvironment as a mechanism for phenotype switching in melanoma.

2024-01-24 | GSE253802 | GEO

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