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

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

PROVIDER: PRJNA857052 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20052700.fastq.gz	Fastqsanger.gz
	SRR20052701.fastq.gz	Fastqsanger.gz
	SRR20052702.fastq.gz	Fastqsanger.gz
	SRR20052703.fastq.gz	Fastqsanger.gz
	SRR20052704.fastq.gz	Fastqsanger.gz

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

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

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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

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

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

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

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.

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

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

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

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

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 driven by low levels of the atypical protein kinase Cs (aPKCs) in the intestinal epithelium. We show here that a salient feature of these tumors is the accumulation of hyaluronan (HA) which, along with reduced aPKC levels, predicts poor survival. HA promotes epithelial heterogeneity and the emergence of a tumor fetal metaplastic cell (TFMC) population endowed with invasive cancer features through a network of interactions with activated fibroblasts. TFMCs are sensitive to HA deposition, and their metaplastic markers have prognostic value. We demonstrate that in vivo HA degradation with a clinical dose of hyaluronidase impairs mCRC tumorigenesis and liver metastasis and enables immune checkpoint blockade therapy by promoting the recruitment of B and CD8+ T cells, including a proportion with resident memory features, and by blocking immunosuppression.

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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