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Identification of the tumour transition states occurring during EMT [ATAC-seq]

ABSTRACT: Identification of the tumour transition states occurring during EMT [ATAC-seq]

PROVIDER: PRJNA434063 | ENA |

REPOSITORIES: ENA

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Identification of the tumour transition states occurring during EMT [ATAC-seq]

Project description:EMT (epithelial-mesenchymal transition) in cancer has been associated with tumour stemness, metastasis and resistance to therapy. It has recently been proposed that, rather than being a binary process, EMT occurs through distinct intermediate states. However,direct in vivo evidence supporting this possibility is still lacking. By screening a large panel of cell surface markers, we identified the existence of multiple tumour subpopulations associated with different EMT stages from epithelial to completely mesenchymal states passing through intermediate hybrid states in skin and mammary primary tumours. Although all EMT subpopulations presented similar tumour propagating cell capacity, they displayed different, invasiveness and metastatic potential. Their transcriptional and epigenetic landscapes defined by RNA-seq and ATAC-seq identified the underlying gene regulatory networks, transcription factors and signalling pathways that control these different EMT transition states. Finally, these tumour subpopulations are localized in different niches that differentially regulateEMT transition states.

2018-02-15 | GSE110584 | GEO

Identification of the tumour transition states occurring during EMT

Project description:Identification of the tumour transition states occurring during EMT

| PRJNA433523 | ENA

Identification of the tumour transition states occurring during EMT

Project description:Identification of the tumour transition states occurring during EMT

| PRJNA434060 | ENA

Identification of the tumour transition states occurring during EMT [RNA-seq]

Project description:EMT in cancer has been associated with tumour stemness, metastasis and resistance to therapy. It has recently been proposed that, rather than being a binary process, EMT occurs through distinct intermediate states. However,direct in vivo evidence supporting this possibility is still lacking. By screening a large panel of cell surface markers, we identified the existence of multiple tumour subpopulations associated with different EMT stages from epithelial to completely mesenchymal states passing through intermediate hybrid states in skin and mammary primary tumours. Although all EMT subpopulations presented similar tumour propagating cell capacity, they displayed different , invasiveness and metastatic potential. Their transcriptional and epigenetic landscapes defined by RNA-seq and ATAC-seq identified the underlying gene regulatory networks, transcription factors and signalling pathways that control these different EMT transition states. Finally, these tumour subpopulations are localized in different niches that differentially regulateEMT transition states.

2018-02-15 | GSE110585 | GEO

Identification of the tumour transition states occurring during EMT [RNA-seq]

Project description:Identification of the tumour transition states occurring during EMT [RNA-seq]

| PRJNA434064 | ENA

Identification of the tumour transition states occurring during EMT [p63 overexpression RNA-seq]

2018-02-15 | GSE110586 | GEO

Identification of the tumour transition states occurring during EMT [p63 overexpression RNA-seq]

Project description:Identification of the tumour transition states occurring during EMT [p63 overexpression RNA-seq]

| PRJNA434065 | ENA

Identification of the tumour transition states occurring during EMT

Project description:scRNAseq of YFP+ Epcam+ and Epcam- skin squamous cell carcinoma cells

2018-04-19 | GSE110357 | GEO

Identification of the tumour transition states occurring during EMT

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

2018-02-15 | GSE110587 | GEO

LSD1 activation promotes inducible EMT programs and modulates the tumour microenvironment in breast cancer

Project description:Complex regulatory networks control epithelial-to-mesenchymal transition (EMT) but the underlying epigenetic control is poorly understood. Lysine-specific demethylase 1 (LSD1) is a key histone demethylase that alters the epigenetic landscape. Here we explored the role of LSD1 in global epigenetic regulation of EMT, cancer stem cells (CSCs), the tumour microenvironment, and therapeutic resistance in breast cancer. LSD1 induced pan-genomic gene expression in networks implicated in EMT and selectively elicits gene expression programs in CSCs whilst repressing non-CSC programs. LSD1 phosphorylation at serine-111 (LSD1-s111p) by chromatin anchored protein kinase C-theta (PKC-θ), is critical for its demethylase and EMT promoting activity and LSD1-s111p is enriched in chemoresistant cells in vivo. LSD1 couples to PKC-θ on the mesenchymal gene epigenetic template promotes LSD1-mediated gene induction. In vivo, chemotherapy reduced tumour volume, and when combined with an LSD1 inhibitor, abrogated the mesenchymal signature and promoted an innate, M1 macrophage-like tumouricidal immune response. Circulating tumour cells (CTCs) from metastatic breast cancer (MBC) patients were enriched with LSD1 and pharmacological blockade of LSD1 suppressed the mesenchymal and stem-like signature in these patient-derived CTCs. Overall, LSD1 inhibition may serve as a promising epigenetic adjuvant therapy to subvert its pleiotropic roles in breast cancer progression and treatment resistance.

2018-01-11 | GSE104754 | GEO

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