Tumor-entrained neutrophils inhibit seeding in the pre-metastatic lung
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ABSTRACT:
PROVIDER: PRJNA144243 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below.
2011-07-25 | GSE30888 | GEO
Project description:Primary tumors have been shown to prepare distal organs for later colonization of metastatic cells by stimulating organ-specific infiltration of bone marrow derived cells. Here we demonstrate that neutrophils accumulate in the lung prior to the arrival of metastatic cells in mouse models of breast cancer. Tumor-entrained neutrophils (TENs) inhibit metastatic seeding in the lungs by generating H(2)O(2) and tumor secreted CCL2 is a critical mediator of optimal antimetastatic entrainment of G-CSF-stimulated neutrophils. TENs are present in the peripheral blood of breast cancer patients prior to surgical resection but not in healthy individuals. Thus, whereas tumor-secreted factors contribute to tumor progression at the primary site, they concomitantly induce a neutrophil-mediated inhibitory process at the metastatic site.
| S-EPMC3172582 | biostudies-literature
Project description:Primary tumors have been shown to prepare distal organs for later colonization of metastatic cells by stimulating organ-specific infiltration of bone marrow-derived cells. Here we demonstrate that neutrophils accumulate in the lung prior to the arrival of metastatic cells in mouse models of breast cancer. Tumor-entrained neutrophils (TENs) inhibit metastatic seeding in the lungs by generating H2O2, and tumor-secreted CCL2 is a critical mediator of optimal anti-metastatic entrainment of G-CSF-stimulated neutrophils. TENs are present in the peripheral blood of breast cancer patients prior to surgical resection but not in healthy individuals. Thus, while tumor-secreted factors contribute to tumor progression at the primary site, they concomitantly induce a neutrophil-mediated inhibitory process at the metastatic site. To follow the earliest transcriptional changes in pre-metastatic tissues, we orthotopically injected 4T1 cells into the mammary fat pad of female nude mice. Control mice were orthotopically injected with PBS. 7 days post tumor engraftment, the mice were sacrificed and thoroughly perfused with ice cold PBS, and lung and liver samples were flash frozen in liquid nitrogen. Following RNA extraction, the lung and liver RNA samples were analyzed on MOE430A2 Affymetrix arrays using R/Bioconductor software.
2011-07-25 | GSE30885 | GEO
Project description:Bone invigorates metastatic seeding
| PRJNA675666 | ENA
Project description:Bone invigorates metastatic seeding [RNA-seq]
| PRJNA674386 | ENA
Project description:We herein examine the transciptioal alteration of a single cell derived MDA-MB-231 subline,SCP21. By retrieving tumor cells inoculated in different sites, we generated multiple mammary fat pad tumor, lung metastases or bone metastasis derived SCP21 sublines. RNA-sequencing uncovered the decreased expression of EZH2 target genes in bone metastases derived cells compared other organ entrained and parental SCP21 cells , suggesting enhanced EZH2 activity. Moreover, such phenotype is reversible upon in vitro culture. As a positive control, bone derived cells were also treated with EZH2 inhibitor, EPZ011989, to confirm the decreased level of EZH2 target genes upon EZH2 inhibition.
2021-04-29 | GSE160773 | GEO
Project description:Primary tumors have been shown to prepare distal organs for later colonization of metastatic cells by stimulating organ-specific infiltration of bone marrow-derived cells. Here we demonstrate that neutrophils accumulate in the lung prior to the arrival of metastatic cells in mouse models of breast cancer. Tumor-entrained neutrophils (TENs) inhibit metastatic seeding in the lungs by generating H2O2, and tumor-secreted CCL2 is a critical mediator of optimal anti-metastatic entrainment of G-CSF-stimulated neutrophils. TENs are present in the peripheral blood of breast cancer patients prior to surgical resection but not in healthy individuals. Thus, while tumor-secreted factors contribute to tumor progression at the primary site, they concomitantly induce a neutrophil-mediated inhibitory process at the metastatic site. This experiment was designed to compare the RNA expression profile in resting (control) neutrophils vs. that of TENs (neutrophils purified from tumor-bearing mice). In addition, we also compared the expression profiles of cultured neutrophils in vitro and treated with CCL2, CCL5 and GCSF.
2011-07-25 | GSE30887 | GEO
Project description:Primary tumours establish metastases by interfering with distinct organs. In pre-metastatic organs, a tumour-friendly microenvironment supports metastatic cells and is prepared by many factors including tissue resident cells, bone marrow-derived cells and abundant fibrinogen depositions. However, other components are unclear. Here, we show that a third organ, originally regarded as a bystander, plays an important role in metastasis by directly affecting the pre-metastatic soil. In our model system, the liver participated in lung metastasis as a leucocyte supplier. These liver-derived leucocytes displayed liver-like characteristics and, thus, were designated hepato-entrained leucocytes (HepELs). HepELs had high expression levels of coagulation factor X (FX) and vitronectin (Vtn) and relocated to fibrinogen-rich hyperpermeable regions in pre-metastatic lungs; the cells then switched their expression from Vtn to thrombospondin, both of which were fibrinogen-binding proteins. Cell surface marker analysis revealed that HepELs contained B220+CD11c+NK1.1+ cells. In addition, an injection of B220+CD11c+NK1.1+ cells successfully eliminated fibrinogen depositions in pre-metastatic lungs via FX Moreover, B220+CD11c+NK1.1+ cells demonstrated anti-metastatic tumour ability with IFNγ induction. These findings indicate that liver-primed B220+CD11c+NK1.1+ cells suppress lung metastasis.
| S-EPMC6034134 | biostudies-literature
Project description:Growth Signaling Autonomy in Circulating Tumor Cells Aids Metastatic Seeding
| PRJNA890663 | ENA
Project description:Primary tumours establish metastases by interfering with distinct organs. In pre-metastatic organs, a tumour-friendly microenvironment supports metastatic cells, and is prepared by many factors including tissue resident cells, bone marrow-derived cells and abundant fibrinogen depositions. However, other components are unclear. Here we show that a third organ, originally regarded as a bystander, plays an important role in metastasis by directly affecting the pre-metastatic soil. In our model system, the liver participated in lung metastasis as a leukocyte supplier. These liver-derived leukocytes displayed liver-like characteristics and, thus, were designated hepato-entrained leukocytes (HepELs). HepELs had high expression levels of coagulation factor X (FX) and vitronectin (Vtn), and relocated to fibrinogen-rich hyperpermeable regions in pre-metastatic lungs; the cells then switched their expression from Vtn to thrombospondin, both of which were fibrinogen-binding proteins. Cell surface marker analysis revealed that HepELs contained B220+CD11c+NK1.1+ cells. In addition, an injection of B220+CD11c+NK1.1+ cells successfully eliminated fibrinogen depositions in pre-metastatic lungs via FX. Moreover, B220+CD11c+NK1.1+ cells demonstrated anti-metastatic tumour ability with IFNγ induction. These findings indicate that liver-primed B220+CD11c+NK1.1+ cells suppress lung metastasis.
| S-SCDT-EMM-2017-08643 | biostudies-other