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Transcriptom analysis of FLT1 regulated genes in metastasis associated macrophages

ABSTRACT: Gene expression changes in metastasis associated macrophage (MAM) with control and FLT1 inhibitory antibody (MF1) were compared using FACS sorted cells from mice bearing pulmonary metastasis of breast tumor cells treated with Ctrl and MF1 antibody

ORGANISM(S): Mus musculus

PROVIDER: GSE68843 | GEO | 2015/05/14

SECONDARY ACCESSION(S): PRJNA283865

REPOSITORIES: GEO

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Transcriptom analysis of FLT1 regulated genes in metastasis associated macrophages

Project description:Gene expression changes in metastasis associated macrophage (MAM) with control and FLT1 inhibitory antibody (MF1) were compared using FACS sorted cells from mice bearing pulmonary metastasis of breast tumor cells treated with Ctrl and MF1 antibody A six chip study using total RNA recovered from metastasis associated macrophages from three separate mice treated with FLT1 inhibitory antibody (MF1) and three separate mice treated with control antibody. Each chip measures the expression level of 42586 genes.

2015-05-14 | E-GEOD-68843 | biostudies-arrayexpress

Transcriptom analysis of differentially regulated genes in metastasis associated macrophages(MAM) compared with lung and spleen resident macrophages

2015-05-15 | GSE68862 | GEO

Transcriptom analysis of differentially regulated genes in metastasis associated macrophages(MAM) compared with lung and spleen resident macrophages

Project description:Gene expression changes in metastasis associated macrophage (MAM) FACS sorted cells from mice bearing pulmonary metastasis of breast tumor cells were compared with lung and spleen resident macrophages sorted from healthy mice using same sorting protocol. A six chip study using total RNA recovered from metastasis associated macrophages from three individual mice and lungs and spleens all from three individual mice. Each chip measures the expression level of 42586 genes.

2015-05-15 | E-GEOD-68862 | biostudies-arrayexpress

Comparison of metastasis-inclined microenvironment (MIM) and metastasis-averse microenvironment (MAM) HCC patients

Project description:To determine the role of the hepatic microenvironment in HCC metastasis, we compared the gene expression profiles of 20 noncancerous surrounding hepatic tissues from two HCC patient groups, those with primary HCC together with venous metastasis which we termed a metastasis-inclined microenvironment (MIM) and those with HCC without detectable metastasis, which we termed a metastasis-averse microenvironment (MAM). There were a total of 20 cDNA microarrays performed, comparing 9 MIM or 11 MAM HCC patient samples to a common reference pool of 8 normal liver tissues.

2010-07-01 | E-GEOD-5093 | biostudies-arrayexpress

Comparison of metastasis-inclined microenvironment (MIM) and metastasis-averse microenvironment (MAM) HCC patients

2006-08-17 | GSE5093 | GEO

Malignant ascites microenvironment induced macrophage reprogramming facilities epithelial ovarian cancer peritoneal metastasis

Project description:Macrophages form a primary immune cells population in tumor tissues and malignant ascites microenvironment (MAM). They can be activated and polarized into tumor-associated macrophages (TAM) by the embedded environment and promote tumor progression and metastasis However, the molecular mechanisms of MAM in macrophage polarization and the effects on epithelial ovarian cancer (EOC) metastatic progression remain elusive. Here, we found that that MAM modulates RhoA-GTPase-F-actin-Hippo signaling cascade in facilitating M2-like macrophage polarization that, in turn, promotes tumor dissemination. PUFA enriched magligant ascites microenvironment promote macrophage lipid oxidative phosphorylation and supression RhoA-GTPase-Yap1 axis. Genetic ablation Yap1 in macrophage exhibited M2-like polarization and enhanced ovrian tumor dissemination. Pharmacology inhibit Mst1/2 could rescue M2-like TAM polarization in MAM and alter the lipid oxidation of macrophages in MAM, more importantly, inhibit ovarian metastatic properties. Through comparasion primary TAM (P-TAM) and metastasis TAM (M-TAM), we proved that Hippo-Yap1 siganl results M-TAM with high M2/M1 ratio. These findings implicate critical functions of PUFA modulate RhoA-Hippo axis in facility TAM polarization and also suggest manipulation of PUFA metabolism or RhoA-Hippo siganl as a therapeutic strategy aganist EOC metastasis.

2024-05-01 | GSE175552 | GEO

A Trial of Camrelizumab Combined With Microwave Ablation and Chemotherapy in the Treatment of Colorectal Cancer Liver Metastasis/Pulmonary Metastasis

Project description:Currently, comprehensive treatments for liver metastasis/pulmonary metastasis that cannot reach NED include systemic chemotherapy, interventional chemotherapy, molecular targeted therapy, immunotherapy, and local treatments (ablation therapy, radiation therapy, etc.) for liver metastases. Combination therapy model of local ablation, systemic chemotherapy, and anti-PD -1 monoclonal antibody hopefully can prolong patient survival. This trial will evaluate the effectiveness and safety of carrelizumab combined with microwave ablation and chemotherapy in the treatment of colorectal cancer liver metastasis/pulmonary metastasis

| 2377681 | ecrin-mdr-crc

Chronic pulmonary bacterial infections facilitate breast cancer lung metastasis with tumor-promoting MHCIIhi neutrophils II

Project description:In order to explore whether the tumor-promoting phenotype of MHCIIhi neutrophils was directly affected by bacterial chronic infection, we isolated MHCIIhi neutrophils cells from the lungs of both of CI tumor-bearing mice and CTRL tumor-bearing mice.

2023-07-04 | GSE218646 | GEO

Pulmonary metastasis in xenograft model after orthotopic implantation

Project description:Metastasis is a major factor for mortality in patients with hepatocellular carcinoma (HCC). Thus, there is a need for predictive biomarker(s) for detecting the tipping point before metastasis, so as to prevent further deterioration. To discover early warning signals of pulmonary metastasis in HCC, we analysed time-series gene expression data in the spontaneous pulmonary metastasis mouse HCCLM3-RFP model with our novel dynamic network biomarker (DNB) method. To simulate tumour growth and metastasis in patient livers, we used the spontaneous pulmonary metastasis mouse model, HCCLM3-RFP, which involves the orthotopic transplanted human HCCLM3 cell line labelled with a stable fluorescent protein.We observed that, hepatic tumours in orthotopic xenograft HCCLM3-RFP mice grew gradually from the second to the fifth week after orthotopic implantation in the primary liver tissue, whereas spontaneous pulmonary metastasis occurredonly at the last time point (the fifth week after orthotopic implantation).Thus, we chose the second, third, fourth, and fifth weeks after orthotopic implantation as observation points to collect liver tumours of five orthotopic xenograft mice at each time point and to assess the whole-genome expression.

2017-06-01 | GSE94016 | GEO

Nidogen 1-enriched extracellular vesicles facilitate extrahepatic metastasis of liver cancer by activating pulmonary lung fibroblasts to secrete tumor necrosis factor receptor 1

Project description:In hepatocellular carcinoma (HCC) patients with extrahepatic metastasis, the lung is the most frequent site of metastasis. However, how the lung microenvironment favors disseminated cells remains unclear. Here, it is found that nidogen 1 (NID1) in HCC cell-derived EVs promoted pre-metastatic niche formation in the lung by enhancing angiogenesis and pulmonary endothelial permeability to facilitate colonization of cells and extrahepatic metastasis. Anti-NID1 antibody was able to block the lung colonization of tumor cells induced by HCC patient-derived EVs. EV-NID1 also activated fibroblasts, which secreted tumor necrosis factor receptor 1 (TNFR1), facilitated lung colonization of tumor cells and augmented HCC cell motility. In the clinical perspective, analysis of serum EV-NID1 and TNFR1 in HCC patients revealed their positive correlation and association with tumor stages suggesting the potential of these molecules as noninvasive biomarkers for the early detection of HCC. Administration of anti-TNFR1 antibody effectively diminished lung metastasis in mice. In conclusion, these results demonstrated the interplay of HCC EVs and activated fibroblasts in pre-metastatic niche formation and how blockage of their functions inhibits distant metastasis to the lungs. This study offers promise for the new direction of HCC treatment by targeting oncogenic EV components and their mediated pathways.

2020-11-17 | PXD019566 | Pride

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