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Evidence that inflammation-associated fibroblasts (IAFs) originate from Edil3 stromal "mesitocytes" in the colon following radiation injury

ABSTRACT: Evidence that inflammation-associated fibroblasts (IAFs) originate from Edil3 stromal "mesitocytes" in the colon following radiation injury

PROVIDER: PRJNA1118758 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29251112.fastq.gz	Fastqsanger.gz
	SRR29251113.fastq.gz	Fastqsanger.gz
	SRR29251114.fastq.gz	Fastqsanger.gz
	SRR29251115.fastq.gz	Fastqsanger.gz
	SRR29251116.fastq.gz	Fastqsanger.gz

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Evidence that inflammation-associated fibroblasts (IAFs) originate from Edil3 stromal "mesitocytes" in the colon following radiation injury

Project description:Stromal cells present in the colon crypt provide proliferation and differentiation signals to the epithelial cells, thereby maintaining their integrity and stimulating the regeneration process. Cancer patients treated for tumors located in the abdominopelvic region may develop radiation proctitis, a condition characterized by a strong mucosal inflammation. In this work, single-cell RNA sequencing approaches were combined with spatial transcriptomics to characterize colonic stromal cells in depth, both in control conditions and in the context of radiation-induced ulceration. The present study identifies a novel stromal marker, Edil3 (EGF-like repeats and discoidin domains 3), which defines the major stromal population of the colon. This population is spatially and functionally distinct from telocytes and trophocytes and is expressed along the crypt with a functional proliferation-differentiation axis . This population, which we propose to name "mesitocytes," cooperates with vascular cells to control inflammation and epithelial proliferation. We demonstrate that radiation-induced ulcerated areas are characterized by the presence of inflammation-associated fibroblasts (IAFs) deriving from mesitocytes.

2024-06-01 | GSE268790 | GEO

Stromal reprogramming by FAK inhibition overcomes radiation resistance to allow for immune priming and response to checkpoint blockade [exp2]

Project description:The effect of radiation therapy (RT) on tumor immunity in PDAC is not well understood. To better understand if RT can prime antigen-specific T cell responses, we analyzed human PDAC tissues and PDAC GEMMs. In both settings, we found little to support evidence of RT-induced T cell priming. Using in-vitro systems, we found tumor stromal components, including fibroblasts and collagen, synergize to both blunt RT efficacy and impair RT-induced interferon signaling. Focal Adhesion Kinase (FAK) inhibition rescued RT efficacy in-vitro and in-vivo, leading to tumor regression, T cell priming, and enhanced long-term survival in PDAC mouse models. Based on these data, we initiated a clinical trial of VS-6063 in combination with SBRT in PDAC patients (NCT04331041). Analysis of PDAC tissues from these patients showed stromal reprogramming mirroring our findings in GEMMs. Finally, the addition of checkpoint immunotherapy to RT and FAKi in animal models led to complete tumor regression and long-term survival.

2022-10-09 | GSE207536 | GEO

A novel small molecule Enpp1 inhibitor improves tumor control following radiation therapy by targeting stromal Enpp1 expression

Project description:Through variation in the cancer cell and their immune infiltrates each tumor represents a unique problem, but therapeutic targets can be found in the shared features. Radiation therapy can change the interaction between the cancer cells and the stroma through release of innate adjuvants including the STING agonist cGAMP. Enpp1 is a phosphodiesterase that can be expressed by cancer cells and can degrade cGAMP. Enpp1 can therefore limit innate adjuvant availability following radiation therapy. We observed that many cancer cells lack Enpp1 expression, but that Enpp1 expression is retained in cells of the tumor stroma and this expression in the tumor stroma limits tumor control by radiation therapy. We demonstrate the efficacy of a novel Enpp1 inhibitor and show that this inhibitor improves tumor control by radiation even where the cancer cells lack Enpp1. We show that the mechanism requires STING and type I IFN receptor expression by non-cancer cells, and is dependent on CD8 T cells as a final effector mechanism of tumor control. This suggests that Enpp1 inhibition may be an effective partner for radiation therapy regardless of whether cancer cells express Enpp1, and identifies a novel therapeutic Enpp1 inhibitor suitable for combination therapies in immuno-oncology.

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Stromal reprogramming by FAK inhibition overcomes radiation resistance to allow for immune priming and response to checkpoint blockade [in vitro]

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Gene expression in murine colon mucosa following activation of stromal Hedgehog signalling

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Stromal reprogramming by FAK inhibition overcomes radiation resistance to allow for immune priming and response to checkpoint blockade [scRNA seq data from mice]

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Gene expression in murine colon mucosa following activation of stromal Hedgehog signalling

Project description:In the intestine, Hedgehog (Hh) signalling orchestrates epithelial homeostasis in a bidirectional loop. Differentiated enterocytes secrete the ligand leading to active downstream signaling exclusively in the stroma. In turn, Hh-driven stromal factors contribute to the control of intestinal stem cell numbers and induce epithelial differentiation. To investigate the consequences of stromal Hh activation on the gene expression level, we performed microarray analysis on full-thickness colonic tissue from Col1a2CreER;Ptch1fl/fl mice (C57BL/6 background). Upon Cre-driven recombination, these mice lack the inhibiting Hh receptor Ptch1 specifically in Col1a2 expressing stroma cells, leading to stroma-specific activation of downstream Hh signaling. RNA was isolated from 1 cm of fresh-frozen whole colonic tissue from Col1a2CreER;Ptch1fl/fl mice (n = 4) and controls (n = 4) starting 1.5 cm from the anus 7 days after administration of 5mg Tamoxifen i.p. to activate Cre. RNA quality was assessed using the Agilent 2200 Tape Station system; RNA integrity numbers (RIN) >8 were considered sufficient. Affymetrix Mouse Gene ST 2.0 arrays were used. Robust multi-array average (RMA) median polish procedures were applied for normalization.

2016-08-02 | E-GEOD-67172 | biostudies-arrayexpress

A novel small molecule Enpp1 inhibitor improves tumor control following radiation therapy by targeting stromal Enpp1 expression

Project description:A novel small molecule Enpp1 inhibitor improves tumor control following radiation therapy by targeting stromal Enpp1 expression

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Large numbers of putative miRNAs originate from DNA transposons and are coincident with a large species radiation in bats.

Project description:Large numbers of putative miRNAs originate from DNA transposons and are coincident with a large species radiation in bats.

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[HPP-2.0] The Comparable Microenvironment Shared by Colorectal Adenoma and Carcinoma: An Evidence of Stromal Proteomics

Project description:we initiated a proteomic project to survey stromal proteins responsive to adenoma and carcinoma of colorectal tissues. Most tissues of adjacent, adenoma, and carcinoma were individually sampled from CRC patients using LCM, after which tissue samples were subjected to proteomic analysis using high-resolution mass spectrometry and individual quantification in data-independent acquisition (DIA) mode. By integrating various datasets and bioinformatic algorithms, the analysis concluded that the epithelial proteomics were CRC stage-dependent, whereas the stromal proteomics in adenoma was comparable with that in carcinoma.

2023-10-17 | PXD046176 |

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