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. Author manuscript; available in PMC: 2022 Apr 1.
Published in final edited form as: Cancer Immunol Res. 2021 Feb 12;9(4):454–469. doi: 10.1158/2326-6066.CIR-20-0433

Figure 5. The PIM1-PPARγ signaling axis regulates cellular metabolism and function of MDSCs.

Figure 5.

(A-B) Ingenuity Pathway Analysis (IPA) (A) and GSEA (B) on bulk RNA sequencing data from WT (n=3) and Pim1−/− (n=3) MDSCs reveal that PPARγ signaling is significantly disturbed in the absence of Pim1. (C) Heatmap showing gene expression of Pparg and its targets in WT and Pim1−/− cells. (D-G) Flow cytometry analyses of CD36 (D-E) and PPARγ (F-G) expression in WT and Pim1−/− cells. (H-L) Metabolic and functional analysis of Pim1-deficient MDSCs following ectopic expression of Pparg. Expression levels of CD36 (H-I), fatty acid uptake (J-K), and in vitro suppression activity (L) were measured by flow cytometry in Pim1−/− BM-MDSCs expressing empty vector (MIT) (n=3) or Pparg (n=3). Data are expressed as mean ± SEM from two experiments and significance was determined by t-test. * p < 0.05, *** p < 0.001.