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Myeloid cells stimulate liver metastasis through downregulation of ANGPTL7 in cancer cells

ABSTRACT: Investigation of the molecular effects of myeloid cells on cancer cells. Myeloid cells were shown to promote metastatic liver progression but the mechanisms involved is unknown. Here we examined gene expression changes in cancer cells upon myeloid cell depletion.

ORGANISM(S): Mus musculus

PROVIDER: GSE60748 | GEO | 2014/08/31

SECONDARY ACCESSION(S): PRJNA259421

REPOSITORIES: GEO

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Myeloid cells stimulate liver metastasis through downregulation of ANGPTL7 in cancer cells

Project description:Investigation of the molecular effects of myeloid cells on cancer cells. Myeloid cells were shown to promote metastatic liver progression but the mechanisms involved is unknown. Here we examined gene expression changes in cancer cells upon myeloid cell depletion. Total RNA was isolated from FACS sorted MC38 colon cancer cells in tumor bearing livers of CD11bDTR transgenic mice after PBS (control) or DT (depletion) treatments.

2014-08-31 | E-GEOD-60748 | biostudies-arrayexpress

TNF-a expression by myeloid cells in ascites regulate colorectal cancer

Project description:Interventions: Colorectal cancer surgery inguinal hernia surgery Primary outcome(s): TNF-a expression by myeloid cells in ascites Study Design: Parallel Non-randomized

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Myeloid-derived suppressor cells promote lung cancer metastasis

Project description:Myeloid-derived suppressor cells promote lung cancer metastasis

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Myeloid-derived Suppressor Cells in Colorectal Cancer

Project description:The aim of the study is to evaluate whether the preoperative level of myeloid-derived suppressor cells is associated with postoperative complications classified by Clavien-Dindo categories. Levels of all MDSC, polymorphonuclear MDSC (PMNMDSC), monocytic MDSC (MMDSC), early-stage MDSC (EMDSC) and monocytic to polymorphonuclear MDSC ratio (M/PMN MDCS) were established and compared in patients with postoperative complications, severe postoperative complications (>= IIIA according to Clavien-Dindo) and severe septic complications.

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Carcinoma-produced factors activate myeloid cells through TLR2 to stimulate metastasis.

Project description: Not available

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Type I Interferon Response in Astrocytes Promotes Brain Metastasis by Enhancing Monocytic Myeloid Cell Recruitment

Project description:Cancer metastasis to the brain is a significant clinical problem. Metastasis is the consequence of favorable interactions between invaded cancer cells and the microenvironment. Here, we demonstrate that cancer-activated astrocytes create a sustained low-level activated type I interferon (IFN) microenvironment in brain metastatic lesions. We further confirm that the IFN response in astrocytes facilitate brain metastasis. Mechanistically, IFN signaling in astrocytes activates C-C Motif Chemokine Ligand 2 (CCL2) production, which further increases the recruitment of monocytic myeloid cells. The correlation between CCL2 and monocytic myeloid cells is confirmed in clinical brain metastasis samples. Lastly, genetically or pharmacologically inhibiting C-C Motif Chemokine Receptor 2 (CCR2) significantly reduces brain metastases. Our study clarifies a pro-metastatic effect of type I IFN in the brain even though IFN response has been considered to have anti-tumor effects. Moreover, this work expands our understandings on the interactions between cancer-activated astrocytes and immune cells in brain metastasis.

2023-03-16 | GSE224302 | GEO

Human KIT+ myeloid cells facilitate visceral metastasis by melanoma

Project description:Metastasis of melanoma significantly worsens prognosis and therefore therapeutic interventions that prevent, or slow metastasis could improve patient outcomes. Here, we show using humanized mice that colonization of distant visceral organs with melanoma is dependent upon a human CD33+CD11b+CD117+ progenitor cell subset comprising <4% of the human CD45+ leukocytes. Metastatic tumor-infiltrating CD33+ cells from patients and humanized (h)NSG-SGM3 mice showed converging transcriptional profiles. Single-cell RNAseq analysis identified a gene signature of a KIT/CD117 expressing CD33+ subset that correlated with decreased overall survival in TCGA melanoma samples. Thus, human CD33+CD11b+CD117+ myeloid cells represent a novel candidate biomarker as well as a therapeutic target for metastatic melanoma.

2021-04-08 | GSE161957 | GEO

Rhodes2019 - Immune-Mediated theory of Metastasis

Project description:Abstract: Accumulating experimental and clinical evidence suggest that the immune response to cancer is not exclusively anti-tumor. Indeed, the pro-tumor roles of the immune system - as suppliers of growth and pro-angiogenic factors or defenses against cytotoxic immune attacks, for example - have been long appreciated, but relatively few theoretical works have considered their effects. Inspired by the recently proposed "immune-mediated" theory of metastasis, we develop a mathematical model for tumor-immune interactions at two anatomically distant sites, which includes both anti- and pro-tumor immune effects, and the experimentally observed tumor-induced phenotypic plasticity of immune cells (tumor "education" of the immune cells). Upon confrontation of our model to experimental data, we use it to evaluate the implications of the immune-mediated theory of metastasis. We find that tumor education of immune cells may explain the relatively poor performance of immunotherapies, and that many metastatic phenomena, including metastatic blow-up, dormancy, and metastasis to sites of injury, can be explained by the immune-mediated theory of metastasis. Our results suggest that further work is warranted to fully elucidate the pro-tumor effects of the immune system in metastatic cancer.

2020-03-28 | BIOMD0000000926 | BioModels

Loss of Lamin A/C in myeloid cells promotes lung metastasis through Gfi-1 and C/EBPe-mediated granulocytic differentiation

Project description:The immune suppressive tumor microenvironment contributes to metastatic spread. In particular, tumor-associated myeloid cells, which differ from normal myeloid cells, suppress cytotoxic T lymphocyte-mediated anti-tumor immunity. However, the underlying molecular mechanisms for tumor-associated myeloid lineage differentiation and functional properties are not well understood. Here we report a lack of Lamin A/C, a nuclear lamina protein associated with chromatin remodeling, in tumor-associated granulocytic myeloid cells. Using mouse models of myeloid specific Lamin A/C knockout, and mouse models of triple negative breast cancer (TNBC), we discovered that the loss of Lamin A/C drives CD11b+Ly6G+ granulocytic lineage differentiation. Mechanistically, loss of Lamin A/C increased H3K4me3 and led to the up-regulation of transcription factors C/EBPe and Gfi-1, which are critical for granulocytic lineage differentiation. In addition, loss of Lamin A/C changes the production of inflammatory chemokines and decreases anti-tumor immunity, leading to increased lung metastasis. Our data provide mechanistic understanding of myeloid lineage differentiation and function in the immune suppressive microenvironment in TNBC metastasis.

2019-12-28 | GSE141124 | GEO

Downregulation of iNOS/NO Promotes Epithelial-Mesenchymal Transition and Metastasis in Colorectal Cancer

Project description:Metastasis is the major cause of cancer-related death in patients with colorectal cancer. Although inducible nitric oxide synthase (iNOS) is a crucial regulator of cancer development and progression, its roles in epithelial-mesenchymal transition (EMT) and the pathogenesis of metastatic colorectal cancer have not been fully investigated. Primary colorectal cancer and liver metastatic tissue specimens were analyzed showing 90% of liver metastatic colorectal cancer with reduced expressions of iNOS compared with 6% of primary colorectal cancer. The Cancer Genome Atlas database analyses via cBioPortal reveal that mRNA expression of iNOS negatively correlated with selected EMT markers in colorectal cancer in a cancer type-dependent manner. The transcriptomic profiling (RNA sequencing data) indicates that iNOS knockdown in SW480 colorectal cancer cells induced an EMT program with upregulated expression of selected stem-cell markers. iNOS knockdown did not alter E-cadherin mRNA expression but re-localized it from membrane to cytoplasm through iNOS-GATA4-Crb2-E-cadherin pathway. iNOS knockdown induced a change in cell morphology, and promoted cell invasion and migration in vitro, and metastasis in vivo.

2022-07-13 | GSE178862 | GEO

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