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Expression of Adipocyte/Macrophage Fatty Acid Binding Protein in Tumor Associated Macrophages Promotes Breast Cancer Progression

ABSTRACT: Identification of A-FABP as a new functional marker for pro-tumor associated macrophages.

ORGANISM(S): synthetic construct Mus musculus

PROVIDER: GSE109703 | GEO | 2018/01/27

REPOSITORIES: GEO

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Expression of Adipocyte/Macrophage Fatty Acid-Binding Protein in Tumor-Associated Macrophages Promotes Breast Cancer Progression.

Project description:Tumor-associated macrophages (TAM) play a critical role in cancer development and progression. However, the heterogeneity of TAM presents a major challenge to identify clinically relevant markers for protumor TAM. Here, we report that expression of adipocyte/macrophage fatty acid-binding protein (A-FABP) in TAM promotes breast cancer progression. Although upregulation of A-FABP was inversely associated with breast cancer survival, deficiency of A-FABP significantly reduced mammary tumor growth and metastasis. Furthermore, the protumor effect of A-FABP was mediated by TAM, in particular, in a subset of TAM with a CD11b+F4/80+MHCII-Ly6C- phenotype. A-FABP expression in TAM facilitated protumor IL6/STAT3 signaling through regulation of the NF?B/miR-29b pathway. Collectively, our results suggest A-FABP as a new functional marker for protumor TAM.Significance: These findings identify A-FABP as a functional marker for protumor macrophages, thus offering a new target for tumor immunotherapy. Cancer Res; 78(9); 2343-55. ©2018 AACR.

| S-EPMC5932212 | biostudies-literature

Circulating adipose fatty acid binding protein promotes obesity associated breast cancer development

Project description:It is still unclear that how obesity increases the risk of breast cancer. To address this question, we used mRNA microarrays to characterize mouse breast tumor EO771 cells treated with mouse recombinant A-FABP protein and compared the data from their controls.

2018-12-26 | GSE102975 | GEO

Adipocyte/macrophage fatty acid-binding proteins contribute to metabolic deterioration through actions in both macrophages and adipocytes in mice.

Project description:Adipose tissue inflammation is a characteristic of obesity. However, the mechanisms that regulate this inflammatory response and link adipose inflammation to systemic metabolic consequences are not fully understood. In this study, we have taken advantage of the highly restricted coexpression of adipocyte/macrophage fatty acid-binding proteins (FABPs) aP2 (FABP4) and mal1 (FABP5) to examine the contribution of these lipid chaperones in macrophages and adipocytes to local and systemic inflammation and metabolic homeostasis in mice. Deletion of FABPs in adipocytes resulted in reduced expression of inflammatory cytokines in macrophages, whereas the same deletion in macrophages led to enhanced insulin signaling and glucose uptake in adipocytes. Using radiation chimerism through bone marrow transplantation, we generated mice with FABP deficiency in bone marrow and stroma-derived elements in vivo and studied the impact of each cellular target on local and systemic insulin action and glucose metabolism in dietary obesity. The results of these experiments indicated that neither macrophages nor adipocytes individually could account for the total impact of FABPs on systemic metabolism and suggest that interactions between these 2 cell types, particularly in adipose tissue, are critical for the inflammatory basis of metabolic deterioration.

| S-EPMC2423863 | biostudies-literature

Expression of Adipocyte/Macrophage Fatty Acid Binding Protein in Tumor Associated Macrophages Promotes Breast Cancer Progression

Project description:Expression of Adipocyte/Macrophage Fatty Acid Binding Protein in Tumor Associated Macrophages Promotes Breast Cancer Progression

| PRJNA431765 | ENA

Adipose Fatty Acid Binding Protein Promotes Saturated Fatty Acid-Induced Macrophage Cell Death through Enhancing Ceramide Production.

Project description:Macrophages play a critical role in obesity-associated chronic inflammation and disorders. However, the molecular mechanisms underlying the response of macrophages to elevated fatty acids (FAs) and their contribution to metabolic inflammation in obesity remain to be fully elucidated. In this article, we report a new mechanism by which dietary FAs, in particular, saturated FAs (sFAs), are able to directly trigger macrophage cell death. We demonstrated that excess sFAs, but not unsaturated FAs, induced the production of cytotoxic ceramides (Cers) in macrophage cell lines. Most importantly, expression of adipose FA binding protein (A-FABP) in macrophages facilitated metabolism of excess sFAs for Cer synthesis. Inhibition or deficiency of A-FABP in macrophage cell lines decreased sFA-induced Cer production, thereby resulting in reduced cell death. Furthermore, we validated the role of A-FABP in promoting sFA-induced macrophage cell death with primary bone marrow-derived macrophages and high-fat diet-induced obese mice. Altogether, our data reveal that excess dietary sFAs may serve as direct triggers in induction of Cer production and macrophage cell death through elevated expression of A-FABP, thus establishing A-FABP as a new molecular sensor in triggering macrophage-associated sterile inflammation in obesity.

| S-EPMC5225136 | biostudies-literature

Epidermal fatty acid binding protein prevents chemical-induced skin tumorigenesis by inhibition of SOX2 expression in keratinocytes

Project description:E-FABP expression in keratinocytes increase interferons, in particualur IFNlamda, expression, which activate P53, a critical tumor suppessor, to inhibit or prevent chemical-induced skin tumorigenesis.

2018-08-30 | GSE109583 | GEO

Macrophage fatty acid oxidation inhibits atherosclerosis progression.

Project description:Atherosclerosis is a chronic disorder of the vessel wall. One key regulator of disease progression is lipid handling in macrophages. However, the role of macrophage mitochondrial-dependent fatty acid β-oxidation (FAO) in atherosclerosis is not well defined. To address this, we focused on carnitine palmitoyltransferase (CPT) 1 and 2, which play an essential role in the transport of long chain fatty acids (FAs) into the mitochondria. Using conditional alleles of these mitochondrial enzymes, we have generated myeloid-specific Cpt1a and Cpt2 knockout mutants (CPT1a M-KO and CPT2 M-KO). In culture, macrophages derived from CPT1a and CPT2 M-KO mice have impaired FAO, enhanced expression of the CD36 scavenger receptor, increased uptake of oxidized low-density lipoprotein (oxLDL), and augmented transformation into cholesterol-rich foam cells. In line with these in vitro observations, in the atherosclerosis-susceptible apolipoprotein E (ApoE) KO background, CPT2 M-KO mice demonstrated augmented atherosclerosis, accompanied by increased accumulation of aortic macrophages with elevated CD36 expression. These data suggest that macrophage FAO is athero-protective and that augmenting FAO may potentially slow atherosclerotic progression.

| S-EPMC9124604 | biostudies-literature

Fatty Acid Binding Protein 5 is a Novel Target in Multiple Myeloma

Project description:To identify protein changes in human myeloma cancer cells resulting from FABP inhibition, we treated GFP+/Luc+MM.1S cells with the single inhibitors (50 µM BMS309405 or 50 µM SBFI-26) or the combination (50 µM of each) for 48 hour, isolated total cell proteins, and performed a mass spectrometry-based proteomic analysis.

2023-01-12 | PXD032829 | Pride

Fatty acid binding proteins contribute to multiple myeloma cell maintenance through regulation of Myc, the unfolded protein response, and metabolism

Project description:Multiple myeloma (MM) is an incurable plasma cell malignancy that causes anemia, osteolysis, hypercalcemia, and organ failure, with only a 53% 5-years survival rate. Herein, we present data demonstrating a novel target in MM: the fatty acid binding protein (FABP) family. In clinical data, FABP5 represented a novel biomarker for more aggressive cancer. FABP inhibitors decreased tumor burden in vitro and in vivo and increased survival in immunocompetent and immunocompromised mouse models. FABP5 was the most highly expressed FABP member in myeloma cells, and the most essential for their survival. CRISPR-Cas9 generated FABP5-KO MM.1S cells showed inhibited growth potential. RNA-sequencing and metabolic analysis identified new pathways of action for the FABPs, including MYC, the unfolded protein response (UPR), and metabolic changes. Collectively, our results demonstrate that FABPs comprise a novel, targetable, and safe, therapeutic avenue for MM and other cancers, and suggest inhibiting FABPs may be worthy of further study.

2022-12-11 | GSE190699 | GEO

Fatty acid binding protein-4 promotes alcohol-dependent hepatosteatosis and hepatocellular carcinoma progression.

Project description:Fatty liver disease (hepatosteatosis) is a common early pathology in alcohol-dependent and obese patients. Fatty acid binding protein-4 (FABP4) is normally expressed in adipocytes and macrophages and functions as a regulator of intracellular lipid movement/storage. This study sought to investigate hepatic FABP4 expression and function in alcoholic liver disease (ALD) and hepatocellular carcinoma (HCC). Using chronic ethanol fed mouse models and patient samples FABP4 expression was analyzed. Human HCC cells, and HCC cells transfected to express CYP2E1, were exposed to ethanol and analyzed for FABP4 expression, or exposed to rhFABP4 (in the absence/presence of ERK, p38-MAPK or JNK1/2 inhibitors) and cell proliferation and migration measured. Hepatosteatotic-ALD mouse models exhibited increased hepatic FABP4 mRNA and protein levels, with FABP4 expression confirmed in hepatocytes. In HCC cells, CYP2E1-dependent ethanol metabolism induced FABP4 expression in vitro and exogenous rhFABP4 stimulated proliferation and migration, effects abrogated by ERK and JNK1/2 inhibition. Increased FABP4 was also detected in ALD/ALD-HCC patients, but not patients with viral hepatitis/HCC. Collectively these data demonstrate ethanol metabolism induces hepatic FABP4 expression and FABP4 promotes hepatoma cell proliferation/migration. These data suggest liver-derived FABP4 may be an important paracrine-endocrine factor during hepatic foci expansion and/or hepatoma progression in the underlying setting of ALD.

| S-EPMC7719965 | biostudies-literature

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