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- W4313373547 abstract "Abstract Myeloid-derived suppressor cells are critical to regulation of immune responses; their accumulation in cancer patients inhibit antitumor immunity and suppress T-cells activity thereby promoting cancer progression and metastases. Metabolic reprogramming has been identified as a crucial factor in modulating MDSCs function; however, how lipid metabolism promotes MDSCs activity during tumor remains unknown. Here we report the upregulation of fatty acid transport proteins (FATP2 and FATP4) enhanced the exogenous uptake of fatty acids resulting in hyperlipidemic MDSCs during tumor. Accumulation of unsaturated fatty acids in GM-CSF-induced MDSCs in-vitro released IL-6, ARG1 and iNOS thereby inhibiting T-cells function. Increased fatty acid uptake in MDSCs induces the expression of FATP2 and FATP4 via activation of STAT3. Interestingly, therapeutic blockade of STAT3 decreased lipid accumulation and repressed FATP2 and FATP4 expression in MDSCs. Also, FATP2 specific inhibitor (Lipofermata) abrogated tumor progression in immunocompetent B16F10-tumor bearing mice in MDSCs dependent manner. Therefore, our data suggests therapeutic manipulation of lipid metabolic signaling pathways in MDSCs could be a promising approach to effective cancer immunotherapy." @default.
- W4313373547 created "2023-01-06" @default.
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- W4313373547 date "2020-05-01" @default.
- W4313373547 modified "2023-10-09" @default.
- W4313373547 title "STAT3 induces the expression of fatty acid transport proteins (FATP2 and FATP4) to promote myeloid-derived suppressor cells function in tumor" @default.
- W4313373547 doi "https://doi.org/10.4049/jimmunol.204.supp.164.9" @default.
- W4313373547 hasPublicationYear "2020" @default.
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