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Single cell analysis of endothelial cells in mouse LLC tumors by STING activation

ABSTRACT: To investigate the trancriptomic changes of endothelial cells (ECs) in response to STING activation, Lewis Lung Carcinoma (LLC) tumor ECs either treated by PBS or cGAMP were sorted by FACS and single-cell RNA seq was performed.

ORGANISM(S): Mus musculus

PROVIDER: GSE159013 | GEO | 2020/10/28

REPOSITORIES: GEO

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Transcriptomic changes of tumor endothelial cells in spontaneous breast tumour model and implanted breast tumour model

Project description:To investigate the trancriptomic changes of tumor endothelial cells (ECs) in response to STING activation, tumor ECs from MMTV-PyMT mouse model or implanted breast tumour model were either treated by PBS or cGAMP were sorted by FACS and single-cell RNA seq was performed.

2021-04-05 | GSE171451 | GEO

Transcriptome changes of endothelial cells in mouse tumor by Nf2/Merlin

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Gene expression in STING-/- MEF cells expressing STING R284S variant

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Transcription profiling of Mus musculus PBS vs IL-5 trerated LLC cells, and LLC vs B16 cells at baseline conditions

Project description:PBS and Il-5 (22 pM) treated LLC and B16 cells were harvested after 24 hours, for comparison between: 1) PBS and IL-5 trerated LLC cells, and 2) btween LLC and B16 cells at baseline conditions.

2010-12-13 | E-MEXP-2490 | biostudies-arrayexpress

ENPP1 is an innate immune checkpoint of the anticancer cGAMP-STING pathway

Project description:ENPP1 expression correlates with poor prognosis in many cancers, and we previously discovered that ENPP1 is the dominant hydrolase of extracellular cGAMP: a cancer-cell-produced immunotransmitter that activates the anticancer STING pathway. However, ENPP1 has other catalytic activities and the molecular and cellular mechanisms contributing to its tumorigenic effects remain unclear. Here, using single cell RNA-seq (scRNA-seq), we show that ENPP1 overexpression drives primary tumor growth and metastasis by synergistically dampening extracellular cGAMP-STING mediated antitumoral immunity and activating immunosuppressive extracellular adenosine (eADO) signaling. In addition to cancer cells, stromal and immune cells in the tumor microenvironment (TME) also express ENPP1 which functions as a gate keeper to block cGAMP sensing in these cells. Enpp1 knockout in both cancer cells and normal tissues slowed primary tumor growth and prevented metastasis in an extracellular cGAMP- and STING-dependent manner. Lastly, an ENPP1 knock-in mutation that selectively abolishes ENPP1’s cGAMP hydrolysis activity phenocopied total ENPP1 knockout, demonstrating that restoration of paracrine cGAMP-STING signaling is the dominant anti-cancer mechanism of ENPP1 inhibition. In summary, selectively blocking ENPP1’s cGAMP hydrolysis activity is a promising therapeutic approach for treating cancer.

2023-08-07 | GSE233659 | GEO

Gene expression profiling of mature dendritic cells from mice s. c. treated with GM-CSF-gene transduced LLC cells (LLC/SeV/GM) or control cells (LLC, LLC/SeV/GFP)

Project description:Irradiated granulocyte macrophage-colony stimulating factor (GM-CSF)-transduced autologous tumor cells induce substantial antitumor immunity through the maturation and migration of dendritic cells (DCs). However, little is known about the key molecules involved in GM-CSF-sensitized DCs (GM-DCs) in tumor draining lymph nodes (TDLNs). We initially confirmed that mice subcutaneously injected with poorly immunogenic syngeneic Lewis lung carcinoma (LLC) cells transduced with Sendai virus encoding GM-CSF (LLC/SeV/GM) significantly rejected the tumor growth. Using microarray expression profiling, we obtained a large number of gene expression data files from GM-DCs and control DCs in TDLNs, and subjected them to network-based cluster analysis and unexpectedly unraveled the expression levels of type I IFNs-related genes specifically expressed in plasmacytoid DCs (pDC) were robustly up-regulated in GM-DCs. In vivo depletion assay showed that pDC-depleted mice treated with subcutaneous LLC/SeV/GM cells abrogated the antitumor effects observed in control mice. Moreover combination use of imiquimod for TLR7 triggering on pDC with irradiated LLC/SeV/GM cells induced a significant therapeutic antitumor effect with marked induction of CD9+ pDC with antitumor phenotype, whereas other control mice groups had only minimal to-modest antitumor responses, implicating that this combined vaccine strategy using imiquimod could be promising for improvement of GM-CSF-induced antitumor immunity. Mouse GM-CSF induced gene expression in mature dendritic cells in tumor draining lymph nodes from C57/BL6N female mouse was measured at 2 days after s.c. tumor challenge with GM-CSF gene-transduced LLC cells (LLC/SeV/GM) or control cells (LLC, LLC/SeV/GFP).

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Cyclic-Di-Nucleotides Trigger ULK1 (ATG1) Phosphorylation of STING to Prevent Sustained Innate Immune Signaling

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2013-10-10 | E-GEOD-51199 | biostudies-arrayexpress

Microarray analysis of T-cell death-associated gene 8 (TDAG8)-mediated gene expression in mouse Lewis lung carcinoma (LLC) cells.

Project description:We previously identified an extracellular pH-sensing G protein-coupled receptor T cell death associated gene 8 (TDAG8) as an extracellular pH sensor of tumor cells that promotes cell growth/survival in vitro and tumor development in vivo. To determine genes regulated by TDAG8 in vitro, mouse Lewis lung carcinoma (LLC) cells stably expressing TDAG8 (TDAG8-LLC cells) and control vector (control LLC cells) were cultured under acidic conditions. Transcriptome microarray analysis using Affymetrix GeneChip Mouse Genome 430 2.0 Arrays was performed with total RNA prepared from these cells. To determine genes regulated by TDAG8 in vitro, mouse Lewis lung carcinoma (LLC) cells stably expressing TDAG8 (TDAG8-LLC cells) and control vector (control LLC cells) were cultured under acidic conditions. Transcriptome microarray analysis using Affymetrix GeneChip Mouse Genome 430 2.0 Arrays was performed with a mixture of equal amounts of total RNA samples from four independent cell cultures.

2012-11-01 | E-GEOD-31776 | biostudies-arrayexpress

STING mediates immune responses in a unicellular choanoflagellate

Project description:To reconstruct the ancestry of animal innate immunity, we have developed the choanoflagellate Monosiga brevicollis, one of the closest living relatives of animals, as a model for studying mechanisms underlying pathogen recognition and immune response. We found that M. brevicollis is killed by exposure to Pseudomonas aeruginosa bacteria and selectively avoids ingesting them. Moreover, M. brevicollis expresses STING, which, in animals, activates innate immune pathways in response to cyclic dinucleotides during pathogen sensing. M. brevicollis STING increases the susceptibility of M. brevicollis to P. aeruginosa-induced cell death and is required for responding to the cyclic dinucleotide 2’3’ cGAMP. Furthermore, similar to animals, autophagic signaling in M. brevicollis is induced by 2’3’ cGAMP in a STING-dependent manner.

2021-05-13 | GSE174340 | GEO

Skeletal muscle transcriptome profile in LLC mice model of cancer cachexia.

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