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

ABSTRACT: 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). Keywords: disease state design

ORGANISM(S): Homo sapiens

PROVIDER: GSE5093 | GEO | 2006/08/17

SECONDARY ACCESSION(S): PRJNA95341

REPOSITORIES: GEO

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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

Homo sapiens

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

| PRJNA95341 | ENA

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

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

Cycad Genotoxin Methylazoxymethanol (MAM) Modulates Cellular Pathways Involved in Cancer and Neurodegenerative Disease

Project description:Methylazoxymethanol (MAM), the genotoxic metabolite of the cycad azoxyglucoside cycasin, induces genetic alterations in bacteria, yeast, plants, insects and mammalian cells, but adult nerve cells are thought to be unaffected. We show that the brains of young adult mice treated with a single systemic dose of MAM display DNA damage (O6-methylguanine lesions) that peaks at 48 hours and decline to near-normal levels at 7 days post-treatment. By contrast, at this time, MAM-treated mice lacking the gene encoding the DNA repair enzyme O6-methylguanine DNA methyltransferase (MGMT), showed persistent O6-methylguanine DNA damage. The DNA damage was linked to cell-signaling pathways that are perturbed in cancer and neurodegenerative disease. These data are consistent with the established carcinogenic and developmental neurotoxic properties of MAM in rodents, and they support the proposal that cancer and neurodegeneration share common signal transduction pathways. They also strengthen the hypothesis that early life exposure to the MAM glucoside cycasin has an etiological association with a declining, prototypical neurodegenerative disease seen in Guam, Japan, and New Guinea populations that formerly used the neurotoxic cycad plant for medicine and/or food. Exposure to environmental genotoxins may have relevance to the etiology of related tauopathies, notably, Alzheimer’s disease, as well as cancer. Mouse brains from eleven-week-old male C57BL6 wild-type and Mgmt-/- mice were exposed to either MAM or Vehicle for 6 hr, 24 hr, 48 hr, 168 hr. Five or six mice per group for a total of 94 mice.

2013-01-10 | E-GEOD-26600 | biostudies-arrayexpress

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 FLT1 regulated genes in metastasis associated macrophages

2015-05-14 | GSE68843 | GEO

TFAM loss induces nuclear actin assembly upon mDia2 malonylation to promote liver cancer metastasis

Project description:The mechanisms underlying cancer metastasis remain poorly understood. Here, we report that TFAM deficiency rapidly and stably induced spontaneous lung metastasis in mice with liver cancer. Interestingly, unexpected polymerization of nuclear actin was observed in TFAM-knockdown HCC cells when cytoskeleton was examined. Polymerization of nuclear actin is causally linked to the high-metastatic ability of HCC cells by modulating chromatin accessibility and coordinating the expression of genes associated with extracellular matrix remodeling, angiogenesis, and cell migration. Mechanistically, TFAM deficiency blocked the TCA cycle and increased the intracellular malonyl-CoA levels. Malonylation of mDia2, which drives actin assembly, promotes its nuclear translocation. Importantly, inhibition of malonyl-CoA production or nuclear actin polymerization significantly impeded the spread of HCC cells in mice. Moreover, TFAM was significantly downregulated in metastatic HCC tissues and was associated with overall survival and time to tumor recurrence of HCC patients. Taken together, our study connects mitochondria to the metastasis of human cancer via uncovered mitochondria-to-nucleus retrograde signaling, indicating that TFAM may serve as an effective target to block HCC metastasis.

2022-06-23 | MTBLS4307 | MetaboLights

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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