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. 2019 Jul 5;20(13):3310. doi: 10.3390/ijms20133310

Figure 1.

Figure 1

This figure shows the relationship between human papillomavirus (HPV) oncoproteins and the molecules from CC cells acting in formatting TAMs. In circulating blood, CCL2 (left) was regulated inversely by E6 or E7 [64], and the less expressed CCL2 recruited fewer monocytes into local tumor tissue [30]; IL-10 was upregulated by E6 or E7 and E6 and E7 were upregulated by IL-10 as a circulation in CC cells [65]; Increasing IL-10 could act in M2 polarization process [44]; Transcriptional factors AP-1 and NFκB targeted genes that act in M2 polarization were upregulated by E6 [38]; CCL2 (right) was expressed individualized [30,40,44,66] and CCL2+ CC cells could promote the M2 polarization [30,40]. The molecules which regulated CCL2 expression that act in M2 polarization was unclear. PGE2 which acted in M2 polarization was upregulated by E5 or E6 or E7 [67,68]; TME, tumor microenvironment; CCL2 is the alternative name of monocyte chemoattractant protein (MCP-1); IL-10, interleukin 10; CC cells, cervical cancer cells.