The interaction between IL-33 and TRIM28 in the regulation of macrophage polarization in an ST2-independent manner

Ovarian cancer is one of the most common gynecological cancers and is known to be an immunogenic tumor. The tumor microenvironment provides optimal condition for the growth of ovarian cancer. Macrophages display a highly functional plasticity in the tumor microenvironment, which can respond to various signals. Switching macrophages’ phenotype is a potential therapeutic strategy. In malignant epithelial ovarian tumors, Interleukin-33(IL-33) highly expressed for increasing tumor grade. Our previous studies showed that IL-33 promotes the polarization of M2 macrophages and tumor grows in vivo by reshaping macrophage metabolism through activating the suppressor of tumorigenicity 2(ST2)-dependent signaling pathway. RNA-seq was total RNA extracted from WT or ST2KO BMDMs stimulated with IL-4 (25 ng/ml) for 24 hours. ChIP-seq assays were performed with SimpleChIP® Plus Enzymatic Chromatin IP Kit with anti-IL-33 and normal goat IgG antibodies. The ChIP-enriched DNA from WT or ST2KO BMDMs was purified for analysis.