The main characteristic of ovarian cancer is early metastasis through peritoneal fluid. Ascites contain a large population of TAMs [
8‐
10], forming a unique microenvironment [
11]. Macrophages can inhibit apoptosis, promote tumor invasion and proliferation, suppress antitumor immune cells and foster tumor angiogenesis [
12,
13]. TAMs in the ovarian cancer are generated from monocytes and resident macrophages. Research has shown that ovarian cancer TAMs are similar to monocyte-derived macrophages [
14], which adopt the M2 phenotype. TAMs promote tumor progression, chemotherapeutic resistance and immunosuppression [
11,
12,
15‐
17]. CD163 and CD206/MRC1, which are strongly expressed on TAMs, are receptors for immunosuppressive molecules and predict the early recurrence of ovarian cancer [
18‐
20]. CD163 and CD206 mRNA expression is also associated with IL-10 levels in ascites, which indicate a shorter relapse free survival (RFS) in patients with ovarian cancer [
21]. The prognosis and survival of ovarian cancer patients are related to the presence of TAMs. Several adverse clinical markers are highly expressed by ovarian cancer TAMs, including CD163, Procollagen C-endopeptidase enhancer 2 (PCOLCE2), IL-6 and IL-10 [
22]. TAMs are the primary secretors of most collagens and the main source of most protease inhibitors and make an important part in the synthesis of extracellular matrix (ECM) proteins [
11]. Macrophages play a crucial role in ECM remodeling and the invasion of ovarian cancer [
14,
20,
23]. TAMs can synthesize chemokine ligand 5 (CCL5), chemokine ligand 8 (CXCL8), and selectively synthesize CCL18, CXCL2 and CXCL3, all of which can attract monocytes/macrophages and promote tumor progression [
24].