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IL17A-induced OPN from tumor cells promotes tumor progression by inducing tissue-resident TAM proliferation via LYVE1 [II]

ABSTRACT: IL17A-induced OPN from tumor cells promotes tumor progression by inducing tissue-resident TAM proliferation via LYVE1 [II]

PROVIDER: PRJNA1068632 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27717363_1.fastq.gz	Fastqsanger.gz
	SRR27717363_2.fastq.gz	Fastqsanger.gz
	SRR27717364_1.fastq.gz	Fastqsanger.gz
	SRR27717364_2.fastq.gz	Fastqsanger.gz
	SRR27717365_1.fastq.gz	Fastqsanger.gz

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IL17A-induced OPN from tumor cells promotes tumor progression by inducing tissue-resident TAM proliferation via LYVE1 [I]

Project description:IL17A-induced OPN from tumor cells promotes tumor progression by inducing tissue-resident TAM proliferation via LYVE1 [I]

| PRJNA1068633 | ENA

IL17A-induced OPN from tumor cells promotes tumor progression by inducing tissue-resident TAM proliferation via LYVE1 [I]

Project description:To further understand the downstream mechanism of IL17/IL17R signaling in tumor cells, we performed transcriptome sequencing analysis of 4T1 cells treated with rIL17A

2024-11-14 | GSE254146 | GEO

IL17A-induced OPN from tumor cells promotes tumor progression by inducing tissue-resident TAM proliferation via LYVE1 [II]

Project description:To further understand the downstream mechanism of IL17/IL17R signaling in tumor cells, we performed transcriptome sequencing analysis of 4T1 cells treated with rIL17A

2024-11-14 | GSE254147 | GEO

microRNA expression during tumor-associated macrophage (TAM) differentiation

Project description:To further analyze the change of microRNA(miRNA) between normal peritoneal macrophage(PEC) and TAM from early tumor(12 days after 4T1 cell injection) or TAM from late tumor(21 days after 4T1 cell injection) , we employed Agilent mouse microRNA microarray Rel 12.0 as a discovery platform to identify miRNAs Total RNA from peritoneal macrophage and TAM of early tumor (tumor formed for 12days after BALB/c mice injected wth 4T1 cell) or TAM of late tumor(tumor formed for 21days after BALB/c mice injected with 4T1 cell) were extracted and analyzed using Agilent mouse microRNA microarray platform, and changes of miRNA were screened out. Agilent mouse microRNA microarray is designed for the profiling of mouse miRNA .627 mouse miRNA and 39 mouse virus-related miRNA can be detected by our microRNA microarray.

2015-03-31 | E-GEOD-67408 | biostudies-arrayexpress

microRNA expression during tumor-associated macrophage (TAM) differentiation

2015-03-31 | GSE67408 | GEO

Rab37-mediated OPN secretion enriches SPP1+ macrophages through autocrine–paracrine signaling to drive lung tumor progression

Project description:Tumor-associated Macrophages (TAMs) are highly plastic immune cells that shape the tumor microenvironment (TME) and influence cancer progression. However, the molecular determinants governing their functional heterogeneity remain incompletely understood. In this study, we identify Rab37 as a key regulator that remodels the states of macrophages within the lung TME. Single-cell RNA sequencing revealed that Rab37 wild-type (WT) tumors were enriched in immunosuppressive Spp1+ TAMs, whereas Rab37 knockout (KO) tumors contained a higher proportion of Thbs1+ TAMs, suggesting Rab37-dependent shifts in macrophage programming. Mechanistically, Rab37 promoted osteopontin (OPN) secretion, which activated STAT3 signaling to establish an autocrine feedback loop that sustained Spp1 expression and induced M2-like polarization. Paracrine OPN signaling further enhanced lung cancer cell proliferation, migration, and invasion. In clinical lung cancer specimens, CD163+/Rab37+/OPN+ TAMs correlated with recurrence and poor survival, and multivariate analysis confirmed their independent prognostic value. Together, these findings demonstrate that Rab37 governs macrophage phenotype and function by orchestrating OPN/STAT3 signaling, thereby reinforcing an immunosuppressive TME and promoting lung cancer progression. Targeting the Rab37–OPN axis may thus represent a promising therapeutic strategy.

2026-01-28 | GSE311076 | GEO

Evolution of TAM gene expression in ID8 tumors

Project description:Gene expression was analyzed in peritoneal macrophages and TAM from mice injected with ID8 ovarian cancer cells intraperitoneally 5 and 21 days after tumor cell injection. 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.

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Characterization of tumor associated macrophages (TAM) in the tumor microenvironment of human melanoma

Project description:Characterization of tumor associated macrophages (TAM) in the tumor microenvironment of human melanoma

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The WDR5-H3K4me3 epigenetic axis regulates OPN expression to compensate PD-L1 function to promote pancreatic cancer immune escape [RNA-seq]

Project description:Two orthotopic pancreatic tumor mouse models were used for ChIP-Seq and RNA-Seq to identify genome-wide dysfunction of H3K4me3 and gene expression. Mouse pancreatic tumors have a genome-wide increase in H3K4me3 deposition as compared to normal pancreas. Osteopontin (OPN) and its receptor CD44 were identified being up-regulated in pancreatic tumors by their promoter H3K4me3 deposition. OPN protein is increased in both tumor cells and tumor-infiltrating immune cells in human pancreatic carcinoma and is inversely correlated with pancreatic cancer patient survival. OPN is primarily expressed in tumor cells and monocytic myeloid-derived suppressor cells (M-MDSCs), whereas PD-L1 is expressed in tumor cells, M-MDSCs, polymorphonuclear MDSCs (PMN-MDSCs) and tumor-associated macrophages. WDR5 is essential for H3K4me3-specific histone methyltransferase activity and OPN expression in tumor cells and MDSCs. Pharmacological inhibition of WDR5 significantly decreased OPN protein level, suppressed pancreatic tumor growth, and significantly increased efficacy of anti-PD-1 immunotherapy in suppression of pancreatic tumor growth in vivo.

2021-07-09 | GSE178676 | GEO

Profiling of tumor-associated macrophages (TAM) after anti-MerTK treatment

Project description:Profiling of tumor-associated macrophages (TAM) after anti-MerTK treatment

| PRJNA490763 | ENA