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Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer I

ABSTRACT: Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer I

PROVIDER: PRJNA857058 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20052637.fastq.gz	Fastqsanger.gz
	SRR20052638.fastq.gz	Fastqsanger.gz
	SRR20052639.fastq.gz	Fastqsanger.gz
	SRR20052640.fastq.gz	Fastqsanger.gz
	SRR20052641.fastq.gz	Fastqsanger.gz

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Similar Datasets

Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer

Project description:Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer

| PRJNA857052 | ENA

Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer II

Project description:Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer II

| PRJNA857057 | ENA

Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer III

Project description:Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer III

| PRJNA857056 | ENA

Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer IV

Project description:Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer IV

| PRJNA857055 | ENA

Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer II

Project description:Mesenchymal colorectal cancer (mCRC) is microsatellite stable (MSS), highly desmoplastic, with CD8+ T cells excluded to the stromal periphery, resistant to immunotherapy, and is driven by low levels of the atypical PKCs (aPKCs). We show here that a salient feature of these tumors is the accumulation of hyaluronan (HA), which along with reduced aPKC levels, predict poor survival. HA promotes epithelial heterogeneity, and the emergence of a fetal metaplastic cell population (TFSC) endowed with invasive cancer features through a network of interactions with activated fibroblasts and components of the immune system. TFSCs are sensitive to HA deposition in vivo and organoids, and their gene expression signature has prognostic value. We demonstrate that in vivo HA degradation with a clinical dose of hyaluronidase impairs mCRC tumorigenesis and enables immune checkpoint blockade therapy by promoting the recruitment of B and CD8+ T cells, including a proportion with resident memory features.

2022-12-16 | GSE207778 | GEO

Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer I

2022-12-16 | GSE207776 | GEO

Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer IV

2022-12-16 | GSE207780 | GEO

Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer III

2022-12-16 | GSE207779 | GEO

Hyaluronan driven by epithelial aPKC deficiency remodels the microenvironment and creates a therapeutic vulnerability in mesenchymal colorectal cancer

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

2022-12-16 | GSE207782 | GEO

Expression data from TGFbeta-treated control or aPKC silenced A549 cells

Project description:Aberrant TGFbeta signalling is a hallmark of epithelial derived tumours. Signalling patterns can depend on the membrane trafficking and internalization of the TGFbeta receptors. Protein kinase C (PKC), particularly the atypical PKC isoforms, alter the trafficking of TGFbeta receptors and can alter TGFbeta induced gene expression. We used microarrays to detail the programme of gene expression underlying TGFbeta induction between control or aPKC silenced A549 cells. Control or aPKC silenced A549 cells were serum starved and treated with TGFbeta for 1 hour. Total RNA was extracted from untreated or TGFbeta treated cells after 8 and 24 hours and analyzed using Affymetrix microarrays. We sought to assess TGFbeta gene expression in aPKC silenced lung cancer cells, as we found that knockdown of aPKC extends TGFbeta signalling as assessed by phospho Smad2 levels. Furthermore, increased expression and oncogenic activity of aPKC (PKCiota) has been reported in lung cancer cells.

2011-01-29 | E-GEOD-26241 | biostudies-arrayexpress

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