CD206 modulates the role of M2 macrophages in theorigin of metastatic tumors

Tumor metastasis is a key factor affecting the life of patients with malignant tumors. For the past hundredyears, scientists have focused on how to kill cancer cells and inhibit their metastasisin vivo, but fewbreakthroughs have been made. Here we hypothesized a novel mode for cancer metastasis. We showthat the phagocytosis of apoptotic tumor cells by macrophages leads to their polarization into the M2phenotype, and that the expression of stem cell related as well as drug resistance related genes wasinduced. Therefore, it appears that M2 macrophages have "defected" and have been transformed intothe initial "metastatic cancer cells", and thus are the source, at least in part, of the distal tissue tumormetastasis. This assumption is supported by the presence of fused cells with characteristics of bothmacrophage and tumor cell observed in the peripheral blood and ascites of patients with ovarian cancer.By eliminating the expression of CD206 in M2 macrophages using siRNA, we show that the growth andmetastasis of tumors was suppressed using bothin vitro cell line and with experimental in vivo mousemodels. In summary, we show that M2 macrophages in the blood circulation underwent a "change of loyalty" to become "cancer cells" that transformed into distal tissue metastasis, which could be suppressed by the knockdown of CD206 expression