Feedback loop between fatty acid transport protein 2 and receptor interacting protein 3 pathways promotes polymorphonuclear neutrophil myeloid-derived suppressor cells-potentiated suppressive immunity in bladder cancer

Pang, Shiyu; Zhou, Jiawei; Yan, Guang; Sun, Jie; Tan, Wanlong

doi:10.1007/s11033-022-07924-x

Cited by 3 publications

(4 citation statements)

References 31 publications

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“…Prospective studies involving tumor necrosis factor-related apoptosis-inducing ligand receptor 2 (TRAIL-R2) agonists have shown selective reduction in PMN-MDSCs 24 . In addition, suppression of fatty acid transport protein 2 (FATP2) weakens the immunosuppressive effect of PMN-MDSCs and creates a new means to specifically target suppressive neutrophils by reducing prostaglandin E2 synthesis 25 . Moreover, ferroptosis inhibitor suppresses the immunosuppressive functions of PMN-MDSCs, thus inhibiting tumor progression in a mouse model 26 .…”

Section: Neutrophil-dependent Therapiesmentioning

confidence: 99%

Neutrophils in the era of single-cell RNA sequencing: functions and targeted therapies in cancer

Qin,

Wei,

Ren

2024

Cancer Biol Med

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Section: Neutrophil-dependent Therapiesmentioning

confidence: 99%

Neutrophils in the era of single-cell RNA sequencing: functions and targeted therapies in cancer

Qin,

Wei,

Ren

2024

Cancer Biol Med

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“…Inhibition of CD36 can reduce the immunosuppressive function of MDSCs [ 218 ]. Similarly, FATP2 can also be overexpressed in PMN-MDSCs, induced by tumor cell-derived GM-CSF and the activation of STAT3 signaling [ 10 , 220 ]. It promotes intracellular PGE2 synthesis and exerts tumor-promoting effects [ 220 ].…”

Section: Landscape and Mechanisms Of Lipid Metabolic Reprogramming In...mentioning

confidence: 99%

“…Similarly, FATP2 can also be overexpressed in PMN-MDSCs, induced by tumor cell-derived GM-CSF and the activation of STAT3 signaling [ 10 , 220 ]. It promotes intracellular PGE2 synthesis and exerts tumor-promoting effects [ 220 ]. Inhibiting FATP2 in MDSCs enhances anti-PD-L1 tumor immunotherapy by upregulating CD107a and decreasing PD-L1 expression on CD8 + TILs [ 221 ].…”

Section: Landscape and Mechanisms Of Lipid Metabolic Reprogramming In...mentioning

confidence: 99%

Lipid metabolic reprogramming in tumor microenvironment: from mechanisms to therapeutics

Jin,

Wang,

Wang

et al. 2023

J Hematol Oncol

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Lipid metabolic reprogramming is an emerging hallmark of cancer. In order to sustain uncontrolled proliferation and survive in unfavorable environments that lack oxygen and nutrients, tumor cells undergo metabolic transformations to exploit various ways of acquiring lipid and increasing lipid oxidation. In addition, stromal cells and immune cells in the tumor microenvironment also undergo lipid metabolic reprogramming, which further affects tumor functional phenotypes and immune responses. Given that lipid metabolism plays a critical role in supporting cancer progression and remodeling the tumor microenvironment, targeting the lipid metabolism pathway could provide a novel approach to cancer treatment. This review seeks to: (1) clarify the overall landscape and mechanisms of lipid metabolic reprogramming in cancer, (2) summarize the lipid metabolic landscapes within stromal cells and immune cells in the tumor microenvironment, and clarify their roles in tumor progression, and (3) summarize potential therapeutic targets for lipid metabolism, and highlight the potential for combining such approaches with other anti-tumor therapies to provide new therapeutic opportunities for cancer patients.

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“…The fatty acid transport protein 2 (FATP2) on PMN-MDSCs through arachidonic acid (AA) uptake and prostaglandin E2 (PGE2) synthesis also support the immunosuppressive function of MDSCs (Figure 5) (182,183). Furthermore, the PGE2-mediated negative feedback loop FATP2 and receptor-interacting protein kinase 3 (RIPK3, A negative regulator of FATP2) promotes PMN-MDSCs' immunosuppressive function (184,185). GM-CSF controls the FATP2 overexpression on PMN-MDSCs in TIME via STAT5 activation.…”

Section: Neutrophils and Myeloid-derived Suppressor Cells Immunometab...mentioning

confidence: 99%

Immunometabolic reprogramming, another cancer hallmark

Kumar

Stewart

2023

Front. Immunol.

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Molecular carcinogenesis is a multistep process that involves acquired abnormalities in key biological processes. The complexity of cancer pathogenesis is best illustrated in the six hallmarks of the cancer: (1) the development of self-sufficient growth signals, (2) the emergence of clones that are resistant to apoptosis, (3) resistance to the antigrowth signals, (4) neo-angiogenesis, (5) the invasion of normal tissue or spread to the distant organs, and (6) limitless replicative potential. It also appears that non-resolving inflammation leads to the dysregulation of immune cell metabolism and subsequent cancer progression. The present article delineates immunometabolic reprogramming as a critical hallmark of cancer by linking chronic inflammation and immunosuppression to cancer growth and metastasis. We propose that targeting tumor immunometabolic reprogramming will lead to the design of novel immunotherapeutic approaches to cancer.

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Feedback loop between fatty acid transport protein 2 and receptor interacting protein 3 pathways promotes polymorphonuclear neutrophil myeloid-derived suppressor cells-potentiated suppressive immunity in bladder cancer

Cited by 3 publications

References 31 publications

Neutrophils in the era of single-cell RNA sequencing: functions and targeted therapies in cancer

Neutrophils in the era of single-cell RNA sequencing: functions and targeted therapies in cancer

Lipid metabolic reprogramming in tumor microenvironment: from mechanisms to therapeutics

Immunometabolic reprogramming, another cancer hallmark

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