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EZH2 inhibtion and IFNy treatment of patient derived organoids [scRNA-Seq]

ABSTRACT: We report the transcriptomics of primary murine lung squamous cell carcinomas in mice treated with EZH2 inhibition and anti-PD1

ORGANISM(S): Mus musculus

PROVIDER: GSE233665 | GEO | 2023/06/01

REPOSITORIES: GEO

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EZH2 inhibtion and IFNy treatment of patient derived organoids [RNA-seq]

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EZH2 inhibtion and IFNy treatment of patient derived organoids

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Affinify Purification of EZH2 and phosphodeficient EZH2 identifies phosphorylation dependent interactions of EZH2

Project description:Overexpression of EZH2 in estrogen receptor negative (ER-) breast cancer promotes metastasis. EZH2 has been mainly studied as the catalytic component of the Polycomb Repressive Complex 2 (PRC2) that mediates gene repression by trimethylating histone H3 at lysine 27 (H3K27me3). However, how EZH2 drives metastasis despite the low H3K27me3 levels observed in ER- breast cancer is unknown. We have shown that in human invasive carcinomas and distant metastases, cytoplasmic EZH2 phosphorylated at T367 is significantly associated with ER- disease and low H3K27me3 levels. Here, we explore the interactome of EZH2 and of a phosphodeficient mutant EZH2_T367A. We identified novel interactors of EZH2, and identified interactions that are dependent on the phosphorylation and cellular localization of EZH2 that may play a role in EZH2 dependent metastatic progression.

2018-07-03 | PXD010073 | Pride

Expression data from patient-derived pancreatic cancer organoids with gene engineering

Project description:Lineage plasticity often emerges in human cancer along with clinical progression and exposure to chemotherapy. Although lineage transition is evident in an aggressive subtype of human pancreatic cancer characterized by the loss of the ductal identity and manifestation of squamous cell-like features, the drivers of these processes have remained elusive. We here harmonized organoid technology, molecular profiling and gene engineering and found that the H3K27me3-mediated erasure of the ductal identity and lineage specifiers, and hijacking of the TP63-driven squamous-cell program provide environmental fitness. Induction and fixation of the squamous-cell identity was dependent on Wnt-deficient environment, whereas KDM6A loss or a hypoxic niche licensed tumor cells for squamous reprogramming. EZH2 inhibition counterbalanced the epigenetic bias and curbed the growth of pancreatic cancer organoids with squamous features. Our results demonstrate how adversarial microenvironment dictates the molecular and histological evolution of human pancreatic cancer, and provide insights into the principles and significance of lineage conversion in human cancer. We used microarray gene expression analysis to study the effect of delta-Np63 overexpression and TP63 knockout in patient-derived pancreatic cancer organoids or genetically engineered organoids.

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