We are analyzing https://link.springer.com/article/10.1186/s12944-023-01807-1.

Title:
Lipid metabolism reprogramming in tumor-associated macrophages and implications for therapy | Lipids in Health and Disease
Description:
The tumormicroenvironment (TME) plays a key role in tumor progression. Tumor-associated macrophages (TAMs), which are natural immune cells abundantin the TME, are mainly divided into the anti-tumor M1 subtype and pro-tumor M2 subtype. Due to the high plasticity of TAMs, the conversion of the M1 to M2 phenotype in hypoxic and hypoglycemic TME promotes cancer progression, which is closely related to lipid metabolism. Key factors of lipid metabolism in TAMs, including peroxisome proliferator-activated receptor and lipoxygenase, promote the formation of a tumor immunosuppressive microenvironment and facilitate immune escape. In addition, tumor cells promote lipid accumulation in TAMs, causing TAMs to polarize to the M2 phenotype. Moreover, other factors of lipid metabolism, such as abhydrolase domain containing 5 and fatty acid binding protein, have both promoting and inhibiting effects on tumor cells. Therefore, further research on lipid metabolism in tumors is still required. In addition, statins, as core drugs regulating cholesterol metabolism, can inhibit lipid rafts and adhesion of tumor cells, which can sensitize them to chemotherapeutic drugs. Clinical studies on simvastatin and lovastatin in a variety of tumors are underway. This article provides a comprehensive review of the role of lipid metabolism in TAMs in tumor progression, and provides new ideas for targeting lipid metabolism in tumor therapy.
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28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

tams, pubmed, tumor, cancer, lipid, cells, metabolism, article, google, scholar, cas, central, macrophages, cholesterol, fatty, cell, acid, immune, tumorassociated, mouse, phenotype, tumors, promotes, protein, promote, expression, human, role, progression, effects, macrophage, receptor, tme, breast, polarization, growth, pathway, accumulation, inhibit, immunosuppression, inhibiting, activation, involving, effect, targeting, promoting, key, proliferation, enhance, fao,

Topics {✒️}

caspase-1/tpparγ/medium-chain acyl-coa dehydrogenase pkc-nf-κb/stat1-irf1 signaling pkc/nf-κb/stat1 axis iκb kinase/nf-κb pathway integrin/fak/erk signaling pathway peroxisome proliferator-activated receptor peroxisome proliferator-activated receptors fatty acid-binding proteins il-4-stat6 pathway-mediated polarization weaken pro-tumorigenic activity article download pdf integrin β3/fak pathway adenosine triphosphate-binding cassette nf-κb-mediated production reduction-responsive rnai nanoplatform upregulating p21cip1/waf1 gene van der touw block sra-mediated adhesion pparγ-mediated lipid metabolism d-amino acid peptide tumor necrosis factor-α macrophages-mediated oxidative stress myeloid-derived suppressor cells arachidonic-acid-derived eicosanoids upregulating nuclear factor-kappa downregulate pd-l1 expression common immune-infiltrating cells exhibit pro-cancer activity effectively agonize pparβ/δ secrete tumor-killing cytokines exert anti-tumor effects exert tumor-killing effects triple-negative breast cancer anti-tumor macrophages activated secrete large amounts abhd5/srm/spermine axis pro-tumor m2 subtype upregulate pd-l1 expression cox-related lipid metabolism enhances cisplatin-induced apoptosis cell-derived interferon-γ upregulates ifn-γ expression srebp1-dependent metabolic fitness triglyceride-related lipid metabolism anti-tumor m1 subtype english language editing promoting ifn-β responses inhibits fao-dependent ros key rate-limiting enzyme nf-κb pathway

Questions {❓}

How do macrophages sense modified low-density lipoproteins?

Schema {🗺️}

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         description:The tumormicroenvironment (TME) plays a key role in tumor progression. Tumor-associated macrophages (TAMs), which are natural immune cells abundantin the TME, are mainly divided into the anti-tumor M1 subtype and pro-tumor M2 subtype. Due to the high plasticity of TAMs, the conversion of the M1 to M2 phenotype in hypoxic and hypoglycemic TME promotes cancer progression, which is closely related to lipid metabolism. Key factors of lipid metabolism in TAMs, including peroxisome proliferator-activated receptor and lipoxygenase, promote the formation of a tumor immunosuppressive microenvironment and facilitate immune escape. In addition, tumor cells promote lipid accumulation in TAMs, causing TAMs to polarize to the M2 phenotype. Moreover, other factors of lipid metabolism, such as abhydrolase domain containing 5 and fatty acid binding protein, have both promoting and inhibiting effects on tumor cells. Therefore, further research on lipid metabolism in tumors is still required. In addition, statins, as core drugs regulating cholesterol metabolism, can inhibit lipid rafts and adhesion of tumor cells, which can sensitize them to chemotherapeutic drugs. Clinical studies on simvastatin and lovastatin in a variety of tumors are underway. This article provides a comprehensive review of the role of lipid metabolism in TAMs in tumor progression, and provides new ideas for targeting lipid metabolism in tumor therapy.
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