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. Author manuscript; available in PMC: 2022 May 28.
Published in final edited form as: Cancer Lett. 2021 Mar 4;506:83–94. doi: 10.1016/j.canlet.2021.02.021

Fig. 5. FGL2-induced CXCL7 production is regulated by the CD16/Syk/PI3K/HIF1α pathway.

Fig. 5.

(A), Blocking FGL2 in mFGL2hi-conditioned media (CM) leads to a decrease in CXCL7 production in BMDMs. F1, F2, F3, F4, and F5 are different hybridoma clones of anti-mFGL2 antibodies. (B), Blocking FGL2 by F5 in hFGL2+-CM leads to a decrease in CXCL7 production in THP-1 macrophages. F4 and F5 are different hybridoma clones of anti-hFGL2 antibodies. ### P < 0.001 vs IgG. (C), Blocking CD16a receptor decreases FGL2-induced CXCL7 production in THP-1 macrophages. (D), Dose-response curve of CXCL7 production. CXCL7 produced by THP-1 macrophages treated with hFGL2+ CM in the presence or absence of different dosages of the HIF1 inhibitor BAY87–2243 (Bay87), pan-HIF inhibitor 2-MeOE2, PI3K/mTOR inhibitor PKI-587 (PKI), MEK1/ERK inhibitor U0126, MEK1/2 inhibitor PD0325901 (PD), MEK1/ERK inhibitor AZD6244 (AZD), or p38 inhibitor PH797804 (PH). (E), Immunoblots for SYK, PI3Kp85, AKT, HIF1α, ERK, and P38 in THP-1 macrophages treated with hFGL2+ CM pretreated with IgG and an anti-FGL2 antibody at the indicated time points. Representative blots are shown in the left. Quantitative analysis of expression is shown in the right. (F), Schematic representation of the crosstalk between glioma cells and glioma-associated macrophages (GAMs). Representative data from 3 independent experiments are shown. **P < 0.01, ***P < 0.001.