Abstract：
:Inflammatory cells such as macrophages can play a pro-tumorigenic role in the tumor stroma. Tumor-associated macrophages (TAMs) generally display an M2 phenotype with tumor-promoting activity; however, the mechanisms regulating the TAM phenotype remain unclear. Complement 5a (C5a) is a cytokine-like polypeptide that is generated during complement system activation and is known to promote tumor growth. Herein, we investigated the role of C5a on macrophage polarization in colon cancer metastasis in mice. We found that deficiency of the C5a receptor (C5aR) severely impairs the metastatic ability of implanted colon cancer cells. C5aR was expressed on TAMs, which exhibited an M2-like functional profile in colon cancer liver metastatic lesions. Furthermore, C5a mediated macrophage polarization and this process relied substantially on activation of the nuclear factor-kappa B (NF-κB) pathway. Finally, analysis of human colon carcinoma indicated that C5aR expression is negatively associated with tumor differentiation grade. Our results demonstrate that C5aR has a central role in regulating the M2 phenotype of TAMs, which in turn, contributes to hepatic metastasis of colon cancer through NF-κB signaling. C5a is a potential novel marker for cancer prognosis and drugs targeting complement system activation, specifically the C5aR pathway, may offer new therapeutic opportunities for colon cancer management.
journal_name
Exp Cell Resjournal_title
Experimental cell researchauthors
Piao C,Zhang WM,Li TT,Zhang CC,Qiu S,Liu Y,Liu S,Jin M,Jia LX,Song WC,Du Jdoi
10.1016/j.yexcr.2018.03.009subject
Has Abstractpub_date
2018-05-15 00:00:00pages
127-138issue
2eissn
0014-4827issn
1090-2422pii
S0014-4827(18)30129-0journal_volume
366pub_type
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journal_title：Experimental cell research
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