Using dynamic cell communication improves treatment strategies of breast cancer

Table 1 Indirect cell communication mediated by metabolites

Signal source	Communication molecules	Signal-receiving cells	Functions	References
Circulation	alpha-Ketoglutarate	breast cancer cells	Stabilize HIF prolyl hydroxylase 2 (PHD2) and decrease HIF-1α, ultimately suppressing breast cancer metastasis	[61]
Circulation	Arachidonic acid	Breast cancer cells	Stimulate the ERK1/2 and PI3K/AKT signaling pathways within endothelial cells to promote angiogenesis and metastasis in breast cancer	[62]
Circulation	Lactate	Breast cancer cells	Activate G protein-coupled receptor 132 (Gpr132) on macrophages to stimulate macrophage differentiation into the M2 phenotype and promote the adhesion, metastasis and invasion of breast cancer cells	[63]
Fibroblast	Kynurenine	Breast cancer cells	FORM complex with Aryl hydrocarbon receptor (AhR) to degrade E-cadherin and increase breast cancer invasiveness	[108]
Circulation	Hydroxycholesterol	Breast cancer cells	Contacts estrogen receptor and liver X receptor to promote the growth and metastasis of breast cancer cells	[109]
Circulation	5α-pregnane-3,20-dione	Breast cancer cells	Increases cell proliferation and detachment	[110]
	Lysophosphatidic acid	Breast cancer cells	Contacts lysophosphatidic acid receptor to contribute to the progression of breast cancer	[111]
Circulation	3,3′-diindolylmethane (DIM)	Breast cancer cells	Aborgates tetrachlorodibenzo(p)dioxin (TCDD)-induced inflammation and tumorigenesis	[112]

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