TAMs upregulate DNMT1 in gastric cancer cells through the CCL5/CCR5/STAT3 pathway. TAMs upregulate DNMT1 in gastric cancer cells through the CCL5/CCR5/STAT3.

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TAMs upregulate DNMT1 in gastric cancer cells through the CCL5/CCR5/STAT3 pathway. TAMs upregulate DNMT1 in gastric cancer cells through the CCL5/CCR5/STAT3 pathway. A, AGS cells and HR cells were treated with CCL5 at different concentrations for 24 hours. DNMT1 expression was measured by Western blotting. Graphs below each blot show the quantification of DNMT protein. *, P < 0.05 versus untreated cells, one-way ANOVA. B, After treatment with CCL5 at the fixed dose of 10 ng/mL for the indicated times in AGS cells and HR cells. DNMT1 expression was analyzed by Western blotting and was quantified. *, P < 0.05; **, P < 0.01 versus the 0 hour time point, one-way ANOVA. C, During coculture with U937 cells for 72 hours, AGS cells and HR cells were treated with neutralizing CCL5 antibodies (α-CCL5). DNMT1 expression was analyzed by Western blotting and was quantified. *, P < 0.05; **, P < 0.01, significant differences between groups, one-way ANOVA. D, AGS and HR cells were treated with maraviroc at the indicated concentrations for 24 hours in the presence of CCL5 (10 ng/mL). DNMT1 expression was analyzed by Western blotting and was quantified. *, P < 0.05; **, P < 0.01; ***, P < 0.001, significant differences between groups, one-way ANOVA. E, AGS cells and HR cells were treated with CCL5 (10 ng/mL) for the indicated time. STAT3 phosphorylation was detected by Western blotting. F, AGS cells and HR cells were pretreated with AG490 (40 μmol/L) or maraviroc (1 μmol/L) for 1 hour followed by CCL5 treatment for 3 hours. STAT3 phosphorylation was measured by Western blotting. G, After AG490 pretreatment for 1 hour, AGS cells and HR cells were treated with CCL5 for 24 hours. DNMT1 expression was analyzed by Western blotting and was quantified. *, P < 0.05, significant differences between groups, one-way ANOVA. H (left), The mixtures of AGS cells and U937 cells were subcutaneously inoculated into nude mice. When the tumor volume reached 125 mm3, treatment with 5-AZA, PCA, or maraviroc began. Representative image of tumors dissected at the end of experiment from different treatment groups is shown. H (right), The graph depicts the growth curves of tumors receiving different treatments. **, P < 0.01; ***, P < 0.001 compared to the control group, two-way ANOVA. I (left), IHC staining of DNMT1 and GSN was performed using the tumors from different treatment groups. I (right), GSN mRNA expression was measured by qPCR in the tumors from different treatment groups. *, P < 0.05 versus the control group, one-way ANOVA. J, Schematic diagram depicts the possible mechanism whereby TAMs promote epigenetic silencing of GSN in gastric cancer cells. Hao-Chen Wang et al. Cancer Immunol Res 2017;5:885-897 ©2017 by American Association for Cancer Research