Table 2 KRAS and metabolism in TME.

From: Oncogenic KRAS mutations drive immune suppression through immune-related regulatory network and metabolic reprogramming

Cancer type

Target

Metabolism type

Immune-related molecules

immune cells

Refs.

PDAC

UGCG

Glycosphingolipids

IFNγ /IFNGR1

NK and CD8 + T cells

[93]

Lung cancer

FASN

Phosphatidylcholines and triacylglycerides

—

—

[94]

PDAC

PPARδ

Lipid metabolism

CCL2/CCR2

Macrophages and MDSCs

[97]

CRC

GGPP

Cholesterol metabolism

IL-10

B cell

[98]

PDAC

CIB1

Glycolysis metabolism

PD-1

CD8 + T cells

[19]

PDAC

HK1/2 and LDHA

Lactate production

—

Macrophages

[105]

CRC

SLC25A22

Glutamate metabolism

CXCL1/CXCR2

MDSC

[109]

Lung cancer

SLC7A5

Glutamine metabolism

mTORC1

—

[111]

  1. PDAC, pancreatic ductal adenocarcinoma, UGCG UDP-glucose ceramide glucosyltransferase, IFNγ interferon-gamma, IFNGR1 interferon gamma receptor 1, NK natural killer cell, FASN fatty acid synthase, PPARδ peroxisome proliferator-activated receptor delta, CCL2 C-C motif chemokine, CCR2 C-C motif receptor 2, MDSCs myeloid-derived suppressor cells, CRC colorectal cancer, GGPP geranylgeranyl pyrophosphate, IL-10 interleukin-10, CIB1 chorionic gonadotropin beta polypeptide 1, PD-1 programmed cell death protein 1, HK1/2 hexokinase 1/2, LDHA lactate dehydrogenase A, SLC25A22 mitochondrial glutamate carrier 1, CXCL1 C-X-C motif ligand 1, CXCR2 C-X-C motif chemokine receptor 2, SLC7A5 solute carrier family 7 member 5, mTORC1 mammalian target of rapamycin complex 1.