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Loss of PRC2 or KMT2D-COMPASS Generates Two Quasi-Mesenchymal Cell States with Distinct Metastatic Abilities

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE158115 | GEO | 2022/02/07

REPOSITORIES: GEO

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Loss of PRC2 or KMT2D-COMPASS Generates Two Quasi-Mesenchymal Cell States with Distinct Metastatic Abilities

Project description:Loss of PRC2 or KMT2D-COMPASS Generates Two Quasi-Mesenchymal Cell States with Distinct Metastatic Abilities

| PRJNA664027 | ENA

Genome-wide CRISPR screen identifies PRC2 and KMT2D-COMPASS as regulators of distinct EMT trajectories that contribute differentially to metastasis.

Project description:Epithelial-mesenchymal transition (EMT) programs operate within carcinoma cells, where they generate phenotypes associated with malignant progression. In their various manifestations, EMT programs enable epithelial cells to enter into a series of intermediate states arrayed along the E-M phenotypic spectrum. At present, we lack a coherent understanding of how carcinoma cells control their entrance into and continued residence in these various states, and which of these states favour the process of metastasis. Here we characterize a layer of EMT-regulating machinery that governs E-M plasticity (EMP). This machinery consists of two chromatin-modifying complexes, PRC2 and KMT2D-COMPASS, which operate as critical regulators to maintain a stable epithelial state. Interestingly, loss of these two complexes unlocks two distinct EMT trajectories. Dysfunction of PRC2, but not KMT2D-COMPASS, yields a quasi-mesenchymal state that is associated with highly metastatic capabilities and poor survival of patients with breast cancer, suggesting that great caution should be applied when PRC2 inhibitors are evaluated clinically in certain patient cohorts. These observations identify epigenetic factors that regulate EMP, determine specific intermediate EMT states and, as a direct consequence, govern the metastatic ability of carcinoma cells.

| S-EPMC9037576 | biostudies-literature

CUT&RUN analysis of PRC2 and KMT2D-COMPASS direct targets in non-convertible HMLER cells

Project description:Analysis of PRC2 and KMT2D-COMPASS binding sequences using CUT&RUN technique in non-convertible HMLER-C1 cells, convertible C2 epithelial cells, as well as C1 EED-KO epithelial and C1-KMT2D-KO epithelial cells.

2022-02-08 | GSE158114 | GEO

Leptomeningeal metastatic cells adopt two phenotypic states.

Project description:BackgroundLeptomeningeal metastasis (LM), or spread of cancer cells into the cerebrospinal fluid (CSF), is characterized by a rapid onset of debilitating neurological symptoms and markedly bleak prognosis. The lack of reproducible in vitro and in vivo models has prevented the development of novel, LM-specific therapies. Although LM allows for longitudinal sampling of floating cancer cells with a spinal tap, attempts to culture patient-derived leptomeningeal cancer cells have not been successful.AimWe, therefore, employ leptomeningeal derivatives of human breast and lung cancer cell lines that reproduce both floating and adherent phenotypes of human LM in vivo and in vitro.Methods and resultsWe introduce a trypsin/EDTA-based fractionation method to reliably separate the two cell subsets and demonstrate that in vitro cultured floating cells have decreased proliferation rate, lower ATP content, and are enriched in distinct metabolic signatures. Long-term fractionation and transcriptomic analysis suggest high degree plasticity between the two phenotypes in vitro. Floating cells colonize mouse leptomeninges more rapidly and associate with shortened survival. In addition, patients harboring LM diagnosed with CSF disease alone succumbed to the disease earlier than patients with adherent (MRI positive) disease.ConclusionTogether, these data support mechanistic evidence of a metabolic adaptation that allows cancer cells to thrive in their natural environment but leads to death in vitro.

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p63/p73 maintain cancer stem cells in a quasi-mesenchymal state and drive metastatic colonization via EGFR signaling

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

2022-11-22 | GSE172407 | GEO

ΔNp63/p73 drive metastatic colonization by controlling a regenerative epithelial stem cell program in quasi-mesenchymal cancer stem cells

Project description:p63/p73 are master transcriptional regulators of ITGB4-hi cancer stem cells and are required to maintain CSCs in a quasi-mesenchymal state and for metastatic colonization

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ΔNp63/p73 drive metastatic colonization by controlling a regenerative epithelial stem cell program in quasi-mesenchymal cancer stem cells

Project description:p63/p73 are master transcriptional regulators of ITGB4-hi cancer stem cells and are required to maintain CSCs in a quasi-mesenchymal state and for metastatic colonization

2022-11-23 | GSE171629 | GEO

ΔNp63/p73 drive metastatic colonization by controlling a regenerative epithelial stem cell program in quasi-mesenchymal cancer stem cells

Project description:p63/p73 are master transcriptional regulators of ITGB4-hi cancer stem cells and are required to maintain CSCs in a quasi-mesenchymal state and for metastatic colonization

2022-11-23 | GSE171628 | GEO

ΔNp63/p73 drive metastatic colonization by controlling a regenerative epithelial stem cell program in quasi-mesenchymal cancer stem cells.

Project description:Cancer stem cells (CSCs) may serve as the cellular seeds of tumor recurrence and metastasis, and they can be generated via epithelial-mesenchymal transitions (EMTs). Isolating pure populations of CSCs is difficult because EMT programs generate multiple alternative cell states, and phenotypic plasticity permits frequent interconversions between these states. Here, we used cell-surface expression of integrin β4 (ITGB4) to isolate highly enriched populations of human breast CSCs, and we identified the gene regulatory network operating in ITGB4+ CSCs. Specifically, we identified ΔNp63 and p73, the latter of which transactivates ΔNp63, as centrally important transcriptional regulators of quasi-mesenchymal CSCs that reside in an intermediate EMT state. We found that the transcriptional program controlled by ΔNp63 in CSCs is largely distinct from the one that it orchestrates in normal basal mammary stem cells and, instead, it more closely resembles a regenerative epithelial stem cell response to wounding. Moreover, quasi-mesenchymal CSCs repurpose this program to drive metastatic colonization via autocrine EGFR signaling.

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p63/p73 maintain cancer stem cells in a quasi-mesenchymal state and drive metastatic colonization via EGFR signaling [ChIP-Seq]

Project description:p63/p73 are master transcriptional regulators of ITGB4-hi cancer stem cells and are required to maintain CSCs in a quasi-mesenchymal state and for metastatic colonization

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