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Macrophage-specific Act1 Knockdown Promoted Adenoma-Adenocarcinoma Transition in Apcmin+/- Mice via Activation of the CXCL9/10-CXCR3 axis

ABSTRACT: Macrophage-specific Act1 Knockdown Promoted Adenoma-Adenocarcinoma Transition in Apcmin+/- Mice via Activation of the CXCL9/10-CXCR3 axis

PROVIDER: PRJNA762555 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15859280_1.fastq.gz	Fastqsanger.gz
	SRR15859280_2.fastq.gz	Fastqsanger.gz
	SRR15859281_1.fastq.gz	Fastqsanger.gz
	SRR15859281_2.fastq.gz	Fastqsanger.gz
	SRR15859282_1.fastq.gz	Fastqsanger.gz

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Macrophage-specific Act1 Knockdown Promoted Adenoma-Adenocarcinoma Transition in Apcmin+/- Mice via Activation of the CXCL9/10-CXCR3 axis

Project description:macrophages involve in colorectal adenocarcinoma transition. Mouse MC38 colorectal cancer cells were co-cultured with BMDM from both anti-Act1 and Wildtype mice. MC38 cells have higher migration speed and express higher EMT markers including Snail, E-cadherins, and Twist after co-culture with anti-Act1 macrophage. Expression profiling by high throughput sequencing highlighted that by co-culturing with MC38 cells, anti-Act1 macrophage increase proinflammatory cytokines secretion and consequently activates cytokines receptor signaling pathway. Specifically, we identified the mechanism where CXCL9/10 from anti-Act1 macrophage interacted with CXCR3 receptor in MC38 cell to promote MC38 migration as well as EMT. Besides, coculturing with MC38 cells enhanced expressions of PD-L1 and MDSCs markers such as Arg1, iNOS, IDO1 in anti-Act1 macrophages. Among activating pathways, we reveal that anti-Act1 macrophage orchestrates NF-kB and STAT3 signaling pathways to upregulate CXCL9/10 secretion and PD-L1 expression. These findings demonstrate that anti-Act1 in macrophage induced a significant shift in MC38 cells gene expression, and modulating the macrophage-cancer is a viable strategy to assist PD-L1 immunotherapy.

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Project description:G protein-coupled receptors (GPCRs) interact with many transducers like G proteins and β-arrestins. Some GPCR agonists act as “biased agonists” which preferentially activate specific signaling transducers over others, leading to unique signaling profiles. The chemokine system, a subfamily of GPCRs that plays a critical role in inflammatory diseases, serves as an endogenous example of biased agonism where over 50 different chemokines ligands and 20 receptors interact promiscuously. In this study, we sought to determine the three different chemokines of the chemkoine receptor CXCR3 generate different transcriptional responses in primary CD8+ T cells. Using RNAseq on CD8+ T cells stimulated with either vehicle control, CXCL9, CXCL10, or CXCL11, the endogenous chemokines of CXCR3, we found that the CXCR3 chemokines promoted unique transcriptional responses that are predicted to differentially regulate inflammatory pathways. We observed significant changes in global transcriptional activation, detecting approximately 48000 transcripts, 887 of which varied by chemokine treatment. There was a high degree of replicability between biological replicates. The overwhelming majority of differentially expressed genes (DEGs) increased in transcript level following chemokine treatment. Compared to vehicle control, CXCL11 demonstrated the largest number of DEGs. Importantly, CXCL11 and CXCL10 demonstrate unique transcriptional profiles where the majority of DEGs were only found following treatment with each specific chemokine, rather than being shared across chemokines. These data contrast with that observed at CXCL9 – although it promoted a significant amount of transcriptional regulation, approximately 66% of CXCL9-induced DEGs were shared with CXCL11 and/or CXCL10.

2022-07-23 | GSE192679 | GEO

Transcriptomic profiling of CXCR3+/- SUM-159-LM1 breast cancer cells

Project description:Cancer-associated fibroblasts promote the development of many primary malignancies, but their function in metastatic progression is poorly understood. Here, we demonstrate that colonization of the lungs by metastatic breast cancer cells induces an inflammatory phenotype in lung fibroblasts. CXCL9 and CXCL10 are induced in an NFκB-dependent manner in metastasis-associated fibroblasts in response IL-1α and IL-1β secreted by disseminated breast cancer cells. We find that the chemokine receptor CXCR3, that binds CXCL9/10, is expressed in a small subset of breast cancer cells that exhibits greater tumor-initiating ability when co-transplanted with fibroblasts. CXCR3-expressing cancer cells maintain JNK signaling that drives IL-1A/B expression, and thus rendering this subpopulation efficient in both inducing CXCL9/10 in lung fibroblasts and responding to the chemokines. Importantly, disruption of the CXCL9/10-CXCR3 axis significantly reduces metastatic colonization in xenograft and syngeneic mouse models suggesting an essential role of this paracrine crosstalk in metastatic progression and a potential therapeutic vulnerability for the treatment of metastatic breast cancer.

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Project description:Background and aims: The transcription factor Stat3 has been considered to promote progression and metastasis of intestinal cancers. Methods: We investigated the role of Stat3 in intestinal tumors using mice with conditional ablation of Stat3 in intestinal epithelial cells (Stat3deltaIEC). Results: In the APCmin mouse model of intestinal cancer, genetic ablation of Stat3 reduced the multiplicity of early adenomas. However, loss of Stat3 promoted tumor progression at later stages leading to formation of invasive carcinomas which significantly shortened the lifespan of Stat3deltaIEC APCmin/+ mice. Interestingly, loss of Stat3 in tumors of APCmin/+ mice had no significant impact on cell survival and angiogenesis but promoted cell proliferation. A genome-wide expression analysis of Stat3-deficient tumors suggested that Stat3 negatively regulates intestinal cancer progression via the cell adhesion molecule Ceacam1. Conclusions: Our data suggest that Stat3 impairs progression of intestinal tumors. Therefore, detrimental effects on tumor progression have to be considered upon therapeutic targeting of the Stat3 signaling pathway in intestinal cancer.

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Single cell changes in RSPO1-Fc treated intestinal adenoma organoids from ApcMin/+ mice

Project description:We constructed AAV-vectors for systemic expression of a soluble RSPO1 protein in ApcMin/+ mice. We found that the RSPO1-Fc fusion protein suppresses the Wnt/ß-catenin signaling activity in intestinal adenomas and in adenoma-derived intestinal organoids ex vivo, but not in normal intestinal epithelial cells. In the Apc mutant cells, the RSPO1-Fc fusion protein activated the TGFß/SMAD signaling pathway to suppress several Wnt target genes and adenoma growth, which effect was rescued suppressed by the TGFß receptor kinase inhibitor SB-431542. Simultaneously, RSPO1-Fc induced proliferation of the normal intestinal stem cells, giving them a growth advantage over the mutant cells, which enabled the intestinal epithelium to eventually outgrow the adenoma cells. Prolonged systemic expression of AAV-RSPO1-Fc decreased significantly the number of the intestinal adenomas and improved the overall survival of ApcMin/+ mice. Thus RSPO1-Fc provides the normal intestinal epithelial cells a growth advantage when compared to the adenoma cells, which eventually leads to the extrusion of the adenomatous tissue. An attractive idea now is to exploit such differential response of normal vs. cancer cells in cancer therapy.

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