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Proteomic Profiling Reveals Differentially Expressed Proteins in TAMs

ABSTRACT: This project aimed to identify differentially expressed proteins between tumor-associated macrophages (TAMs) and monocyte-derived macrophages (MDMs), both obtained from hepatocellular carcinoma (HCC) patients. Macrophages were isolated from tumor tissues and matched peripheral blood, respectively. Proteins were extracted and analyzed by mass spectrometry to characterize their distinct proteomic profiles. The results provide valuable insights into the molecular differences between TAMs and MDMs, contributing to a better understanding of macrophage function and regulation in the HCC tumor microenvironment.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Lysate, Macrophage

DISEASE(S): Hepatobiliary System Cancer

SUBMITTER: Jie Liu

LAB HEAD: Peng Xia

PROVIDER: PXD058385 | Pride | 2025-09-28

REPOSITORIES: Pride

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Project description:Progression and relapse-free survival of ovarian carcinoma are associated with the abundance of immunosuppressed CD163highCD206high tumor-associated macrophages (TAMs) and high levels of polyunsaturated fatty acids (PUFAs), in particular arachidonic acid (AA), in the tumor microenvironment. In the present study, we have investigated whether both associations are functionally linked. Methods: The effect of PUFAs on cytokine-mediated pro-inflammatory signal transduction was studied in primary monocyte-derived macrophages (MDMs) by transcriptomics, bioinformatics, phosphoprotein analysis of signal transduction proteins and MS-based proteomics of lipid rafts. Results: Pathway analysis of transcriptional profiles revealed that high CD163 and CD206/MRC1 expression in TAMs is strongly associated with an inhibition of cytokine-triggered signal transduction. This is mirrored by an impairment of the transcriptional response to interferon-beta (IFNbeta), IFNgamma and IL-6 in monocyte-derived macrophages (MDMs) by AA. This AA-mediated inhibition of pro-inflammatory signaling is caused by dysfunctions of the cognate receptors, as indicated by the inhibition by PUFAs of JAK1, JAK2, STAT1 and STAT3 phosphorylation, with the strongest inhibitory effects exerted by AA and its non-metabolizable analog ETYA. AA/ETYA treatment of MDMs results in altered composition of lipid rafts, including reduced amounts of the interferon receptor IFNAR1, STAT1 and other immune-regulatory proteins. The AA-mediated inhibition of IFN-triggered STAT1 phosphorylation was reversed by water-soluble cholesterol, known to prevent the perturbation of lipid raft structure by PUFAs. Conclusion: Our data suggest that AA, and to a lesser degree other PUFAs, impair pro-inflammatory signaling in macrophages, at least in part by altering the structure of lipid rafts, and thereby contribute to the reeducation of tumor-associated macrophages. Our findings also suggest that the pharmacologic restoration of lipid raft functions in TAM may be a promising strategy for the development of new therapeutic approaches.

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Proteomic Profiling Reveals Differentially Expressed Proteins in TAMs

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