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Table 1 Reprogramming of lipid metabolism in the TME and it plays an important role in diseases

From: Reprogramming of lipid metabolism in the tumor microenvironment: a strategy for tumor immunotherapy

Immune cells

Indicators of lipid metabolism

Mechanisms

Diseases

References

TAM

FABP5

Enhance FAO, oxidative phosphorylation and activate PPAR-γ signaling

Allergic airway inflammation

[20]

FASN

Promote PPAR-δ activation and IL-10 release

Lung cancer

[21]

CD36

Promote the uptake of LDs and LCFAs. Enhance the polarization of M2-TAMs

Liver metastases

[22]

PPAR

Promote FAO and the synthesis of M2-TAMs

HCC

[23]

25-hydroxycholesterol

Activate TLR4 and nuclear factor-κB signaling

Atherosclerosis

[83]

APOA1

ABCG1

Promote cholesterol efflux

Atherosclerosis

[84]

Asprosin

Activate the p38/Elk-1 axis. Promote cholesterol efflux and inhibit lipid accumulation

Atherosclerosis

[84]

CD8 + T

CD36

Promote uptake of FAs and FAO. Inhibit the release of IFN-γ, PRF1, GZMB, and TBX21

Promote uptake of oxLDL and P38 activation

-

[3132]

very long-chain acyl-CoA dehydrogenase

Increases the very long-chain FA accumulation and FAO

PDAC

[39]

Cholesterol

Increasing ER stress and decrease GZMB, IFN-γ, and TNF-α levels

B16 and MC38 tumor models

[35]

LA

Enhance the formation of ER–mitochondrial contacts

-

[38]

SCFAs

Promote the production of CD25, IFN-γ and TNF-α

Pancreatic cancer model

[39]

Treg

CPT1A

Promote FAO and Treg differentiation

-

[42]

CD36

Activate the PPAR-β pathway and promote lipid uptake

-

[40]

FABP5

increase OXPHOS and promote lipid metabolism

-

[45]

SREBP、FASN

inhibit FA synthesis and reduce cholesterol metabolism

-

[46]

DC cells

ACC

Increase the amount of DC lipids

-

[52]

TDE、PPAR-α

Promote OXPHOS

B16/F10 melanoma model

[53]

CD36

Increase lipid accumulation and phagocytosis by DCs

-

[54, 55]

FASN、LPA

Increased FA synthesis and lead to FA accumulation in DCs

Ovarian cancer

[56, 57]

Scavenging receptors

Promote lipid accumulation and decrease cytokine levels

HCC

[58]

CPT1A

Enhance FAO and promotes Treg development

Melanoma

[51]

LDs

Decrease the ability of DCs to activate T cells

Malignant mesothelioma

[59]

NK cells

lipid transporters and enzymes

Inhibit granase B and interferon production. Diminish NK effects

-

[62]

MSR1

CD6

CD36

lipid accumulation

Melanoma, breast, colorectal cancer

[63, 64]

lipids

Transfer lipids into NK-cell exosome-like vesicles and lead to NK cell dysfunction

Breast cancer and lung metastasis

[65]

Cholesterol

SREBP2

Induce FAO

-

[66]

long-chain acylcarnitine

Promote iNK T-cell senescence, cell cycle arrest, and telomere damage

HBV-associated HCC

[67]

MDSCs

ApoE

Promotes neutrophil senescence

Prostate tumor

[71]

PMN-MDSCs

FATP2

Increase lipid accumulation

Colon, pancreas, and lymphatic system cancers

[73, 74]

XBP1

Promotes cholesterol synthesis and secretion

-

[75]

CAFs

LPC

Create lysophosphatidic acid and accelerate tumor growth

PDAC

[79]

FATP1

Increase the intake of exogenous FAs

Triple-negative breast cancer

[60]

CD36

promotes lipid peroxidation and p38 phosphorylation,

HCC

[80]