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. 2021 Sep 15;11:727306. doi: 10.3389/fonc.2021.727306

Figure 4.

Figure 4

CALM2 overexpression aggravated GC cell-mediated angiogenesis and macrophage polarization. (A) IHC was operated to assess the profiles of CD163, CD206, and CD11b in GC tissues (data from the Human Protein Atlas). (B) CALM2’s affinities with CD163, CD206, and CD11b in GC tissues were analyzed through Person regression analysis. THP1 cells stimulated by PMA were co-cultured with the conditioned medium of GC cells. (C) CCK8 monitored macrophage proliferation. (D) Transwell investigated macrophage migration. (E, F) The profiles of M2-type macrophage surface receptors CD206, CD163, and CD11b and M1-type macrophage markers CD80, CD86, and iNOS were figured out via Western Blot. (G) The mRNA expressions of M2-type macrophage-concerned factors CXCL12, IL-4, IL-13, IL-10, and VEGFA were confirmed through qRT-PCR. HUVECs were co-cultured with the conditioned medium of GC cells. (H) The viability of HUVECs was examined by CCK8. (I) HUVEC angiogenesis was checked by tubule formation experiment. (J) HUVECs’ migration was assessed through the wound scratch test. Statistics were presented as mean ± SD (n=3). *P < 0.05, **P < 0.01, ***P < 0.001 (vs. the Blank group). &P < 0.05, &&P < 0.01 (vs. the CM+Vector group).