Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Target macrophage SPP1 promotes CD8 T cell infiltrations

ABSTRACT: SPP1 in tumor associated macrophages (TAM) can inhibit the infiltration of CD8 T cells, promote tumor growth, and reduce the efficacy of ICI immunotherapy. RNA sequencing data showed diffrential expressed genes and enrichment pathway in the bone marrow derived macrophages from SPP1fl/fl-Lyz2-icre mice compared to control SPP1fl/fl mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE297153 | GEO | 2026/06/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Target macrophage SPP1 promtes CD8 T cell infiltrations

Project description:SPP1 in tumor associated macrophages (TAM) can inhibit the infiltration of CD8 T cells, promote tumor growth, and reduce the efficacy of ICI immunotherapy. Single cell (sc)-RNA sequencing data showed markedly increased CD8 T cells in the tumor tissues of SPP1fl/fl-Lyz2-icre mice compared to control SPP1fl/fl mice.

2026-06-30 | GSE296902 | GEO

SPP1 represents a therapeutic target that promotes the progression of esophageal squamous cell carcinoma by driving M2 macrophage infiltration

Project description:Background: Tumor-associated macrophages (TAMs) are an important component of the tumor microenvironment (TME). However, the crosstalk between esophageal squamous cell carcinoma (ESCC) cells and TAMs remains largely unexplored. Methods: Clinical samples and the TCGA database were used to evaluate the relevance of SPP1 and TAM infiltration in ESCC. Mouse models were constructed to investigate the roles of macrophages educated by SPP1 in ESCC. Macrophage phenotypes were determined using qRT‒PCR and immunohistochemical staining. RNA sequencing was performed to elucidate the mechanism. Results: Increasing expression of SPP1 correlated with M2-like TAM accumulation in ESCC, and they both predicted poor prognosis in the ESCC cohort. Knockdown of SPP1 significantly inhibited the infiltration of M2 TAMs in xenograft tumors. In vivo mouse model experiments showed that SPP1-mediated education of macrophages plays essential roles in the progression of ESCC. Mechanistically, SPP1 recruited macrophages and promoted M2 polarization via CD44/PI3K/AKT signaling activation and then induced VEGFA and IL6 secretion to sustain ESCC progression. Finally, blockade of SPP1 with RNA aptamer significantly inhibited tumor growth and M2 TAM infiltration in xenograft mouse models. Conclusions: This study highlights a SPP1-mediated crosstalk between ESCC cells and TAMs in ESCC. SPP1 could serve as a potential target in ESCC therapy.

2024-09-09 | GSE256360 | GEO

Proteomic changes in the colon of mice with epithelial specific deletion of Apc or Apc/Dhps

Project description:C57BL/6 mice with a tamoxifen (TAM)-inducible disruption of Apc (CDX2P-CreERT2;Apc fl/fl) or Apc and Dhps (CDX2P-CreERT2;Apc fl/fl;Dhps fl/fl) were injected or not with one intraperitoneal injection 4.5 mg/kg TAM. After 35 days, the following colon biopsies were harvested: normal tissues from mice that did not receive TAM, non-tumor tissues from mice treated with TAM, and tumors from mice treated with TAM. Biopsies from 5 mice were collected for the following sample groups: (1) Apc Control; (2) Apc/Dhps Control; (3) Apc+TAM non-tumor; (4) Apc/Dhps+TAM non-tumor; (5) Apc+TAM tumor; (6) Apc/Dhps+TAM tumor

2025-09-12 | PXD061596 | Pride

mRNA transcriptome sequencing of siglecf low macrophages from tumor lungs of chimeric mice that were intranasally injected with Ad-Cre

Project description:The transcriptional profiling of siglecf low macrophages from tumor lungs of Tmem173fl/fl→KrasLSL-G12D/+Lkb1fl/fl (WTKL) and Tmem173fl/fl;Lyz2-Cre→KrasLSL-G12D/+Lkb1fl/fl (LYZKL) chimeric mice.

2025-11-29 | GSE301096 | GEO

Study of Spp1 Knock out in brain macrophages compare to wild type mice

Project description:Embryonic brain macrophages from Wild type or Spp1 KO mice embryo E14.5 and E18.5 were analysed by single cell RNA sequencing

2024-02-27 | E-MTAB-13581 | biostudies-arrayexpress

The Cellular and Molecular Origin of Tumor-associated Macrophages

Project description:Long recognized as an evolutionarily ancient cell type involved in tissue homeostasis and immune defense against pathogens, macrophages are being rediscovered as regulators of several diseases including cancer. Here we show that in mice, mammary tumor growth induces the accumulation of tumor-associated macrophages (TAMs) that are phenotypically and functionally distinct from mammary tissue macrophages (MTMs). TAMs express the adhesion molecule Vcam1 and proliferate upon their differentiation from inflammatory monocytes, but do not exhibit an “alternatively activated” phenotype. TAM differentiation depends on the transcriptional regulator of Notch signaling, RBPJ; and TAM, but not MTM, depletion restores tumor-infiltrating cytotoxic T cell responses and suppresses tumor growth. These findings reveal the ontogeny of TAMs and a discrete tumor-elicited inflammatory response, which may provide new opportunities for cancer immunotherapy. MMTV-PyMT mice (Jackson Laboratory) were backcrossed to the C57BL/6 background for 10 generations. Rbpjfl/fl mice were provided by Tasuku Honjo and crossed to CD11ccre mice provided by Boris Reizis. Littermate controls were used in all experiments when possible. All mice were maintained in a specific pathogen-free facility and animal experimentation was conducted in accordance with institutional guidelines. In the MMTV-PyMT spontaneous mammary tumor model, we found the key Notch transcriptional regulator, RBPJ, to be required for TAM terminal differentiation from inflammatory monocytes. The bulk myeloid cell population that remains in CD11cCreRbpj fl/fl mice (the cells in "Rbpj KO" samples), represents monocytes that have begun their differentiation into macrophages, but are unable to terminally differentiate due to the lack of Rbpj.

2014-04-18 | E-GEOD-56755 | biostudies-arrayexpress

Regulation ot TAM gene expression by ABCA1 and ABCG1 (4 Cre- and 4 Cre+)

Project description:Gene expression was analyzed in TAM from mice injected with ID8 ovarian cancer cells intraperitoneally in ABC a1/g1 fl/fl-LysM-Cre mice. Tumor-associated macrophages (TAM) have been shown to have important roles in the malignant progression of various cancers. However, macrophages also posses intrinsic tumoricidal activity and can promote the activity of cytotoxic lymphocytes, but they rapidly adopt an alternative phenotype within tumors, associated with immune-suppression and trophic functions that support tumor growth. The mechanisms that promote TAM polarization in the tumor-microenvironment remain poorly understood, these mechanisms may represent important therapeutic targets to block the tumor-promoting functions of TAM and restore their anti-tumor potential. Here we have characterized TAM in a mouse model of metastatic ovarian cancer. We show that ovarian cancer cells promote membrane-cholesterol efflux and the depletion of lipid rafts from macrophages. Increased cholesterol efflux promoted IL-4 mediated reprogramming while inhibiting IFNg-induced gene expression. These studies reveal an unexpected role for tumor-induced membrane-cholesterol efflux in driving the IL-4 signaling and the tumor-promoting functions of TAM, while rendering them refractory to pro-inflammatory stimuli. Thus, preventing cholesterol efflux in TAM could represent a novel therapeutic strategy to block pro-tumor functions and restore anti-tumor immunity.

2019-02-05 | GSE126079 | GEO

Single-cell RNA sequencing reveals cellular heterogeneity in lineage specification of MC38 subcutaneous tumor cells with either SPP1 overexpression or vector control

Project description:SPP1 (secreted phosphoprotein 1), also known as osteopontin, has emerged as a pivotal factor in the tumor microenvironment (TME) across various cancers. It has been reported that SPP1-positive macrophages are associated with immunosuppressive activity and poor prognosis in colorectal cancer (CRC). The increasing proportion of SPP1-positive macrophages contributes to immune suppression and immune desert by inhibiting T cell function in liver metastatic lesions. However, the role of SPP1 in colorectal cancer liver metastasis (CRLM) remains incompletely understood. Therefore, the impact of tumor-secreted SPP1 on the CRC microenvironment warrants further investigation. To explore the effect of SPP1 on diverse TME cell populations, we conducted single-cell RNA sequencing on MC38 xenografts. Our results revealed an increase in fibroblasts and a concurrent decrease in T cells following SPP1 overexpression, suggesting that SPP1 promotes cancer-associated fibroblast (CAF) infiltration into the CRC TME.

2025-09-24 | GSE298348 | GEO

CD47 Expression in Solid Tumors Correlates with Phagocytic Tumor-Associated Macrophage Gene Signature

Project description:CD47 is a “don’t eat me” signal that is frequently overexpressed in tumors to evade phagocytosis by tumor associated macrophages (TAM). Investigational agents targeting CD47, such as magrolimab, aim to induce phagocytosis of tumor cells by TAMs. Previously, two functionally defined key TAM subsets have been identified: complement C1q C chain positive (C1QC) TAMs, which display pro-phagocytic activity, and secreted phosphoprotein 1 positive (SPP1) TAMs that express pro-angiogenic markers. Here we characterize CD47 expression and its relationship with tumor macrophages in solid tumor samples.

2025-09-04 | GSE296861 | GEO

RNA-Seq to profile transcriptomes in colonic macrophages from Tle3KO (Tle3fl/fl, Lyz2-Cre), Tle4KO (Tle4fl/fl, Lyz2-Cre) and WT (Lyz2-Cre) mice

Project description:RNA-Seq to profile transcriptomes in colonic macrophages from Tle3KO (Tle3fl/fl, Lyz2-Cre), Tle4KO (Tle4fl/fl, Lyz2-Cre) and WT (Lyz2-Cre) mice

| PRJNA759761 | ENA

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