Abstract
Tumor-associated macrophages (TAMs) promote cancer progression via stimulating angiogenesis, invasion/metastasis, and suppressing anti-cancer immunity. Targeting TAMs is a potential promising cancer therapeutic strategy. Neddylation adds the ubiquitin-like protein NEDD8 to substrates, and thereby regulates diverse biological processes in multiple cell types, including macrophages. By controlling cellular responses, the neddylation pathway regulates the function, migration, survival, and polarization of macrophages. In the present review we summarized how the neddylation pathway modulates Macrophages and its implications for cancer therapy.
Highlights
The tumor microenvironment (TME) comprises multiple cell types, including tumor cells, endothelial cells, fibroblasts and immune cells, interacting with each other continuously (Junttila and de Sauvage, 2013)
A recent study from our group showed that the elevated neddylation pathway in cancer cells led to the accumulation of NF-κB-regulated activation of chemokines C motif chemokine ligand 2 (CCL2) with promotion of macrophage infiltration (Zhou et al, 2019a)
IL-4 stimulation resulted in the M2 phenotype (CD11b+/F4/80+/CD206+), while MLN4924 up-regulated the number of M2 macrophages following IL4 treatment (Figure 5D), indicating that inactivation of the neddylation pathway by MLN4924 polarized macrophages toward a M2 phenotype in vitro
Summary
Tumor-associated macrophages (TAMs) promote cancer progression via stimulating angiogenesis, invasion/metastasis, and suppressing anti-cancer immunity. Targeting TAMs is a potential promising cancer therapeutic strategy. Neddylation adds the ubiquitin-like protein NEDD8 to substrates, and thereby regulates diverse biological processes in multiple cell types, including macrophages. The neddylation pathway regulates the function, migration, survival, and polarization of macrophages. In the present review we summarized how the neddylation pathway modulates Macrophages and its implications for cancer therapy
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