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Effect of ∆Np63 deletion on plasticity of post-injury lung basal cells

ABSTRACT: Effect of ∆Np63 deletion on plasticity of post-injury lung basal cells

PROVIDER: PRJNA892466 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21981224_1.fastq.gz	Fastqsanger.gz
	SRR21981224_2.fastq.gz	Fastqsanger.gz
	SRR21981225_1.fastq.gz	Fastqsanger.gz
	SRR21981225_2.fastq.gz	Fastqsanger.gz
	SRR21981226_1.fastq.gz	Fastqsanger.gz

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Effect of ∆Np63 deletion on plasticity of post-injury lung basal cells

Project description:Basal cells were isolated from an influenza-infected non-tamoxifen treated Krt5CreERT2; RFP; ∆Np63flox/flox mouse and cultured, allowing for inducible ∆Np63 deletion in vitro. These basal cells were plated as monolayers, airway organoids, and alveolar organoids and treated with 1uM 4OHT for +4OHT (∆Np63 KO) or equivalent volume DMSO for -4OHT (solvent only, ∆Np63 WT). Technical triplicates of ∆Np63 WT and ∆Np63 KO were harvested for each growth condition for RNA sequencing.

2022-11-11 | GSE216160 | GEO

Effect of ∆Np63 deletion on epigenomic rewiring via differential H3K27ac and H3K27me3 enrichment

Project description:Basal cells were isolated from an influenza-infected non-tamoxifen treated Krt5CreERT2; RFP; ∆Np63flox/flox mouse and cultured, allowing for inducible ∆Np63 deletion in vitro. These basal cells were plated as monolayers and treated with 1uM 4OHT for +4OHT (∆Np63 KO) or equivalent volume DMSO for -4OHT (solvent only, ∆Np63 WT) for 48 hours. Technical triplicates of ∆Np63 WT and ∆Np63 KO treated in parallel were harvested for each IP for p63 and each histone modification for ChIP-seq.

2022-11-11 | GSE216159 | GEO

Loss of ∆Np63 induces epigenetic rewiring and enhances plasticity towards alveolar identity

Project description:Loss of ∆Np63 induces epigenetic rewiring and enhances plasticity towards alveolar identity

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Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas

Project description:Basal breast cancers, an aggressive breast cancer subtype that has poor treatment options, are thought to arise from luminal mammary epithelial cells that undergo basal-like plasticity through poorly understood mechanisms. Using genetic mouse models and ex vivo primary organoid cultures, we show that conditional co-deletion of the LATS1 and LATS2 kinases, key effectors of Hippo pathway signaling, in mature mammary luminal epithelial cells promotes the development of basal-like carcinomas that metastasize over time. Genetic co-deletion experiments revealed that phenotypes resulting from the loss of LATS1/2 activity are dependent on the transcriptional regulators YAP/TAZ. Notably, transcriptional analyses of LATS1/2-deleted mammary epithelial cells revealed a gene expression program that associates with human basal breast cancers. Our study demonstrates in vivo roles for the LATS1/2 kinases in mammary epithelial homeostasis and luminal-basal fate control and implicates signaling networks induced upon the loss of LATS1/2 activity in the development of basal breast cancers.

2022-09-26 | GSE196555 | GEO

∆Np63 regulates stem cell activity in mammary gland development

Project description:MaSC, luminal progenitor enriched subpopulations and total MECs as well, were isolated from both wild type and ∆Np63 KO heterozygous mouse and the transcriptome profiles were determined and compared. Three populations: P4, P5 and MECs; two genotypes: WT vs ∆Np63 heterozygous.

2014-08-19 | E-GEOD-47417 | biostudies-arrayexpress

Effect of ∆Np63 deletion on epigenomic rewiring via differential H3K27ac and H3K27me3 enrichment

Project description:Effect of ∆Np63 deletion on epigenomic rewiring via differential H3K27ac and H3K27me3 enrichment

| PRJNA892467 | ENA

∆Np63 executes an oncogenic program through the regulation of a common landscape of super-enhancer associated genes in non-small cell lung cancer

Project description:Distinct lung stem cells give rise to lung adenocarcinoma (ADC) and squamous cell carcinoma (SCC). ΔNp63 guides development of these cells through regulation of terminal differentiation; however, its mechanistic role in lung cancer development has remained elusive. We utilized a ΔNp63-specific conditional knockout mouse model and found that ∆Np63 maintains lung ADC and SCC by keeping lung stem cells in quiescence. ChIP-seq analysis of lung basal cells and alveolar type 2 (AT2) cells lacking ∆Np63 revealed a robust loss of activating histone marks at super enhancers of cell identity genes defining a unifying oncogenic role for ∆Np63 in non-small cell lung cancer.

2021-12-23 | GSE131671 | GEO

A USP28-∆Np63 axis is a druggable vulnerability of squamous tumour formation and maintenance

Project description:The oncoprotein ∆Np63 is an essential transcriptional master- and cell identity regulator in squamous cell carcinoma (SCC) of various origins, encompassing lung, head and neck, oesophagus, cervix and skin. While in non-transformed cells ∆Np63 protein abundance is tightly regulated by the ubiquitin proteasome system (UPS), in tumours E3-ligases ubiquitylating ∆Np63, such as FBXW7, are commonly mutated or lost, resulting in a hyper-stabilisation of the oncogenic driver. Targeting ∆Np63 protein abundance in SCC could present a possible therapeutic avenue. Here, we report that the deubiquitylase USP28 regulates ∆Np63 protein stability and abundance in SCC by counteracting the degradative UPS system. Interference with USP28 activity by pharmacological inhibition specifically affected human SCC cell lines and, finally, we were able to demonstrate in vivo using CRISPR/Cas9 mouse models that Usp28 is required for SCC induction and maintenance. Hence, targeting USP28 is a viable option to tackle ∆Np63 protein abundance in SCC tumours.

2020-03-04 | GSE129982 | GEO

delta-Np63 loss of function study in the HNSCC cell line UT-SCC-74A

Project description:delta-Np63 is highly expressed in squamous cell carcinoma of the head and neck (HNSCC). To evaluate its function in HNSCC we depleted delta-Np63 by siRNAs in the HNSCC cell line UT-SCC-74A. The transcriptome was analysed by cDNA microarray.

2016-01-14 | E-MTAB-3670 | biostudies-arrayexpress

Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas

Project description:Inactivation of LATS1/2 drives luminal-basal plasticity to initiate basal-like mammary carcinomas

| PRJNA805501 | ENA