Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Symbiotic Adhesion of Neutrophils and Epithelial-like Cancer Cells Shapes the Tumor Microenvironment and Promotes Metastasis [1] [coculture]

ABSTRACT: Neutrophils play complicated roles in tumor progression. Examination of several murine triple negative breast cancer (TNBC) models revealed nearly opposite impact of neutrophils on epithelial-like vs. mesenchymal-like cancer cells (ECCs vs. MCCs). Interaction with ECCs upregulates ICAM1 in neutrophils, a feature that also distinguishes tumor-infiltrating neutrophils from other neutrophils in human. Direct adhesion between ECCs and neutrophils, especially the ICAMhigh subpopulation, promote the survival of each other – forming a symbiotic relationship. In contrast, MCCs are thwarted by neutrophils due to decreased cell adhesion and elastase resistance. The ICAM1high neutrophils are known for reverse migration to circulation. The adhesive and reverse migratory properties of ICAM1high neutrophils mediate intravasation of metastatic seeds. These observations were verified in a subset of human TNBCs that unexpectedly enrich non-Hispanic European patients. Thus, we demonstrated a co-evolution through which neutrophils sculpt phenotypes and metastatic behaviors of TNBC, which may preferentially occur in patients of certain race/ethnicity.

ORGANISM(S): Mus musculus

PROVIDER: GSE284277 | GEO | 2026/05/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Diverse impact of neutrophils on cancer cells of different epithelial/mesenchymal phenotypes leads to distinct tumor microenvironment and metastatic behavior [3]

Project description:Neutrophils play complicated roles in tumor progression. Examination of several murine triple negative breast cancer (TNBC) models revealed nearly opposite impact of neutrophils on epithelial-like vs. mesenchymal-like cancer cells (ECCs vs. MCCs). Interaction with ECCs upregulates ICAM1 in neutrophils, a feature that also distinguishes tumor-infiltrating neutrophils from other neutrophils in human. Direct adhesion between ECCs and neutrophils, especially the ICAMhigh subpopulation, promote the survival of each other – forming a symbiotic relationship. In contrast, MCCs are thwarted by neutrophils due to decreased cell adhesion and elastase resistance. The ICAM1high neutrophils are known for reverse migration to circulation. The adhesive and reverse migratory properties of ICAM1high neutrophils mediate intravasation of metastatic seeds. These observations were verified in a subset of human TNBCs that unexpectedly enrich non-Hispanic European patients. Thus, we demonstrated a co-evolution through which neutrophils sculpt phenotypes and metastatic behaviors of TNBC, which may preferentially occur in patients of certain race/ethnicity.

2026-05-21 | GSE284279 | GEO

Symbiotic Adhesion of Neutrophils and Epithelial-like Cancer Cells Shapes the Tumor Microenvironment and Promotes Metastasis [2]

2026-05-19 | GSE284278 | GEO

ICAM1high Neutrophils Sculpt Tumor Evolution and Metastasis through Symbiotic Adhesion and Reverse Migration

Project description:Analyses of neutrophils of pan human cancers revealed an ICAM1high subset enriched in the tumor microenvironment, mMurine triple negative breast cancer (TNBC) models recapitulate this observation. ICAM1high neutrophils exhibited enhanced capacity of cell-cell adhesion specifically with tumor cells retaining epithelial features, and this adhesion confers mutual advantages on both cell types. In contrast, cancer cells of mesenchymal-like phenotypes are thwarted by neutrophils due to decreased cell adhesion and elastase resistance. These nearly opposite effects drive the evolution toward a dichotomy of neutrophil-enriched, epithelial-like versus macrophage-enriched, mesenchymal-like ecosystems. The ICAM1high neutrophils are known for reverse migration (from tissue to circulation). The adhesive and reverse migratory properties together mediate metastatic intravasation. These observations were verified in a subset of human TNBCs that unexpectedly enrich in non-Hispanic European patients. Thus, we demonstrated a co-evolution through which neutrophils sculpt phenotypes and metastatic behaviors of TNBC, which may preferentially occur in patients of certain race/ethnicity.

2026-05-19 | GSE319442 | GEO

ICAM1high Neutrophils Sculpt Tumor Evolution and Metastasis through Symbiotic Adhesion and Reverse Migration

Project description:Analyses of neutrophils of pan human cancers revealed a ICAM1high subset enriched in the tumor microenvironment, Murine triple negative breast cancer (TNBC) models recapitulate this observation. ICAM1high neutrophils exhibited enhanced capacity of cell-cell adhesion specifically with tumor cells retaining epithelial features, and this adhesion confers mutual advantages on both cell types. In contrast, cancer cells of mesenchymal-like phenotypes are thwarted by neutrophils due to decreased cell adhesion and elastase resistance. These nearly opposite effects drive the evolution toward a dichotomy of neutrophil-enriched, epithelial-like versus macrophage-enriched, mesenchymal-like ecosystems. The ICAM1high neutrophils are known for reverse migration (from tissue to circulation). The adhesive and reverse migratory properties together mediate metastatic intravasation. These observations were verified in a subset of human TNBCs that unexpectedly enrich non-Hispanic European patients. Thus, we demonstrated a co-evolution through which neutrophils sculpt phenotypes and metastatic behaviors of TNBC, which may preferentially occur in patients of certain race/ethnicity.

2026-05-22 | GSE301335 | GEO

Next-generation sequencing to define the impact of metastatic prostate cancer on neutrophils

Project description:Purpose: Prostate cancer most frequently metastasizes to bone and is incurable. Metastatic prostate cancer cells thrive in bone through molecular regulation of surrounding bone stroma; however, it is unclear how non-metastatic vs. metastatic cancer differentially alter the bone cells. Since neutrophils are the most abundant stromal cell in bone, the goal of this study was to identify prostate cancer-induced transcriptomic changes in bone marrow neutrophils for comparison to non-metastatic prostate cancer cells.

2022-08-03 | GSE193468 | GEO

Neutrophil expression array

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

Triple-Negative Breast Cancer Shapes the Systemic Immune Landscape and Alters Neutrophil Functionality [bulkRNA-seq]

Project description:Cancer dysregulates intratumoral innate-adaptive immune cell crosstalk, but it remains largely unknown how the systemic immune landscape is modified during breast cancer progression. Here, we comprehensively profiled the circulating immune profile of patients with stage I-III or stage IV triple-negative breast cancer (TNBC) and healthy donors (HDs). We showed that patients with metastatic TNBC (mTNBC) exhibited decreased numbers of circulating T cells, dendritic cell subsets and differentiated B cells compared to patients with stage I-III TNBC and HDs, which was partially associated with prior chemotherapy. Moreover, increased IL17 production by vδ1 γδ T cells was observed in patients with mTNBC compared to HDs. Classical monocytes and neutrophils were increased in patients with mTNBC compared to HDs, irrespective of prior chemotherapy. Transcriptional and proteomic analysis, alongside ex vivo functionality assays, revealed increased migratory capacity, increased abundance of granule proteins, and elevated ROS production in circulating neutrophils from mTNBC patients. Some of these systemic immune alterations, including decreased levels of non-switched B cells and increased migratory capacity of neutrophils, were already evident in patients with stage I-III TNBC. Our data underscore the significant impact of TNBC disease stage on the systemic immune composition and function.

2025-01-25 | GSE264108 | GEO

Triple-Triple-Negative Breast Cancer Shapes the Systemic Immune Landscape and Alters Neutrophil Functionality

Project description:Cancer dysregulates intratumoral adaptive-innate immune cell crosstalk, however, it remains largely unknown how the systemic immune landscape is modified during breast cancer progression and whether prior chemotherapy treatment exerts persistent changes on circulating immune cells. Here, we comprehensively profiled the systemic immune landscape in patients with triple negative breast cancer (TNBC) at distinct disease stages, to understand how cancer progression and treatment history shape the systemic immune landscape. We performed multi-parameter flow cytometry analysis to assess the global systemic immune landscape, including often overlooked granulocytes. We showed that patients with metastatic TNBC (mTNBC) exhibited increased classical monocytes and neutrophils compared to healthy donors (HDs) irrespective of prior therapy. Conversely, circulating T cells, dendritic cell subsets and differentiated B cells were reduced in patients with mTNBC compared to HDs, which could partially be attributed to prior chemotherapy treatment. Phenotypic and functional characterization of the T cell compartment revealed increased IL17 production by vδ1 γδ T cells, were increased. Transcriptional and proteomic analysis, alongside ex vivo functionality assays, revealed increased migratory capacity, increased granule proteins, and elevated ROS production in circulating neutrophils of mTNBC patients. Our data demonstrate that patient neutrophils are not only more abundant, but also display an altered functionality, underscoring the significant impact of TNBC disease stage and treatment history on the systemic immune composition and function.

2025-04-09 | PXD051334 | Pride

METTL3 modulates cell viability and motility in HCC1143 and MDA-MB-231 triple-negative breast cancer cell lines

Project description:The m6A methyltransferase METTL3 functions as a critical oncogenic driver in triple negative breast cancer (TNBC). However, its specific downstream targets and mechanistic functions in less metastatic TNBC subtypes remain poorly characterized. To address this, we evaluated METTL3 expression and the phenotypic effects of its siRNA-mediated knockdown in healthy mammary epithelial (MCF10A), low-metastatic TNBC (HCC1143) and high-metastatic TNBC (MDA-MB-231) cell lines. We assessed global m6A levels, cell proliferation, cell cycle progression and migration. To uncover specific downstream pathways, transcriptomic profiling was performed on HCC1143 cells, followed by RT-qPCR validation and m6A site prediction. METTL3 depletion reduced global m6A levels and cell viability across all cell lines. Notably, in low-metastatic HCC1143 cells, METTL3 knockdown induced a pronounced G2/M cell cycle arrest and dramatically impaired migration capacity. Transcriptomic analysis of HCC1143 revealed altered expression of genes associated with these observed phenotypic changes. Specifically, critical transcripts harboring predicted m6A motifs, including LIMK1, CCNB2 and CDH1, were significantly dysregulated, pointing to potential alterations in pathways governing cytoskeletal remodeling, actin organization, and cell-cell adhesion. Taken together, we propose that METTL3 promotes cellular proliferation and motility in low-metastatic TNBC by regulating key transcripts involved in cell cycle progression and actin dynamics.

2026-04-17 | GSE325029 | GEO

Uridine Phosphorylase-1 supports metastasis by altering immune and extracellular matrix landscapes

Project description:Understanding mechanisms that facilitate early events in metastatic seeding is key to developing therapeutic approaches to reduce metastasis. We have identified uracil as a prominent metastasis-associated metabolite in genetically engineered mouse models of cancer and in patients with metastatic breast cancer. Uracil is generated by the enzyme uridine phosphorylase-1 (UPP1), and we find that neutrophils are a significant source of UPP1 in metastatic cancer. UPP1 increases expression of adhesion molecules on the neutrophil surface, leading to decreased neutrophil motility in the pre-metastatic lung. UPP1-expressing neutrophils suppress T cell proliferation, and the UPP1 product uracil increases fibronectin deposition in the extracellular microenvironment. Consistently, knockout or inhibition of UPP1 in mice with mammary tumours increases T cell numbers and reduces fibronectin content in the lung and decreases the proportion of mice that develop lung metastasis. These data indicate that UPP1 influences neutrophil behaviour and extracellular matrix deposition in the lung and suggest that circulating uracil could be a marker of metastatic disease, and that pharmacological inhibition of UPP1 could be a strategy to reduce metastasis.

2025-03-04 | MSV000097229 | MassIVE

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data