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Gene expression signature in CAFs dependent on PGE2

ABSTRACT: Gene expression signature in CAFs dependent on PGE2

PROVIDER: PRJNA716203 | ENA |

REPOSITORIES: ENA

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Gene expression signature in CAFs dependent on PGE2

Project description:We studied the impact of a PGE2 signaling on tumor progression in the PyMT mammary carcinoma mouse model. To gain insight into the reasons underlying altered tumor development, whole transcriptome profiling of FACS-isolated cancer-associated fibroblasts (CAFs) from WT and mPGES-1 KO tumors were generated via next generation mRNA sequencing, in triplicates, on a NextSeq 550 high-throughput bench top sequencer.

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Identification of the molecular signature of distinctive breast cancer associated fibroblasts (CAFs)

Project description:Cancer associated fibroblasts (CAFs) are highly heterogeneous and different subsets of CAFs may exhibit distinct functions, To identify the molecular signature of distinctive CAFs , we compared mRNA expression profiles of CAFs isolated from tumors in sensitive patients and resistant ones before neo-adjuvant chemotherapy. Compared the CAFs from sensitive samples, those from refractory samples exhibited a distinctive signature.

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Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to PGE2

Project description:Metabolic engagement is intrinsic to immune cell function. Prostaglandin E2 (PGE2) has been shown to modulate macrophage activation, yet how PGE2 might affect metabolism is unclear. Here we show that PGE2 causes mitochondrial membrane potential (Δψm) to dissipate in interleukin-4 activated macrophages (M(IL-4)). Effects on Δψm are a consequence of PGE2-initiated transcriptional regulation of genes in the malate-aspartate shuttle (MAS), particularly GOT1. Reduced Δψm causes alterations in the expression of 126 voltage regulated genes (VRGs) including Resistin like molecule-α (RELMα), a key marker of M(IL-4), and genes that regulate cell cycle, The transcription factor ETS variant 1 (ETV1) plays a role in the regulation of 38% of the VRGs. These results reveal ETV1 as a Δψm-sensitive transcription factor, and Δψm as a mediator of mitochondrial-directed nuclear gene expression.

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Transcription profiling of mouse cancer associated fibroblasts (CAFs) reveals are activation in incipient neoplasia to orchestrate tumor promoting inflammation in an NF-I?B-dependent manner.

Project description:Full title: Cancer Associated Fibroblasts are activated in incipient neoplasia to orchestrate tumor promoting inflammation in an NF-ÎºB-dependent manner. Cancer Associated Fibroblasts (CAFs) support tumorigenesis by stimulating angiogenesis, cancer cell proliferation, and invasion. We demonstrate that CAFs also mediate tumor-enhancing inflammation. Using a mouse model of squamous skin cancer, we found a pro-inflammatory gene signature in CAFs isolated from dysplastic skin. This signature was also evident in CAFs from skin as well as mammary and pancreatic tumors in mice, and in human cancer. Surprisingly, the inflammatory signature was already activated in CAFs isolated from the incipient hyperplastic stage in multistep tumorigenesis. CAFs from this pathway functioned to promote macrophage recruitment, neovascularization and tumor growth in vivo, activities abolished when NF-ÎºB signaling was inhibited. Additionally, we show that normal dermal fibroblasts can be âeducatedâ by carcinoma cells to express pro-inflammatory genes. Experiment Overall Design: We performed expression profiling analysis of dermal fibroblasts sorted from dysplastic skin tissue of K14-HPV16 mice, and from age matched non transgenic controls. This array analysis was repeated in triplicate. Amplified RNA was hybridized to the 430 2.0 Affymetrix mouse genome arrays.

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CAFs are activated in incipient neoplasia to orchestrate tumor promoting inflammation in an NF-κB-dependent manner.

Project description:Full title: Cancer Associated Fibroblasts are activated in incipient neoplasia to orchestrate tumor promoting inflammation in an NF-κB-dependent manner. Cancer Associated Fibroblasts (CAFs) support tumorigenesis by stimulating angiogenesis, cancer cell proliferation, and invasion. We demonstrate that CAFs also mediate tumor-enhancing inflammation. Using a mouse model of squamous skin cancer, we found a pro-inflammatory gene signature in CAFs isolated from dysplastic skin. This signature was also evident in CAFs from skin as well as mammary and pancreatic tumors in mice, and in human cancer. Surprisingly, the inflammatory signature was already activated in CAFs isolated from the incipient hyperplastic stage in multistep tumorigenesis. CAFs from this pathway functioned to promote macrophage recruitment, neovascularization and tumor growth in vivo, activities abolished when NF-κB signaling was inhibited. Additionally, we show that normal dermal fibroblasts can be “educated” by carcinoma cells to express pro-inflammatory genes.

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