Fig. 3: Loss of CDK8 enhances TNBC’s visibility to NK cells. | Cell Death & Disease

Fig. 3: Loss of CDK8 enhances TNBC’s visibility to NK cells.

From: Triple-negative breast cancer cells rely on kinase-independent functions of CDK8 to evade NK-cell-mediated tumor surveillance

Fig. 3

A Heatmap of differentially expressed genes between untreated or Senexin B-treated E0771 control cells and shCdk8-1 or shCdk8-2 cell lines in the KEGG pathway “Natural killer cell-mediated cytotoxicity” (RNA sequencing data; n = 3 replicates). B–E Median fluorescence intensity (MFI) and representative histograms of (B) MHC I (H-2K + H-2D), (C) RAE1 (pan), (D) ICAM-1, and (E) CD274 (PD-L1) expression of E0771 control, shCdk8-1, and shCdk8-2 cells; expression levels of NK ligands were analyzed by flow cytometry. Bar graphs represent technical triplicates (mean ± SEM). F IL-2-expanded C57BL/6 NK cells were incubated for 4 h with CFSE-labeled E0771 control or shCdk8-1/shCdk8-2 tumor cells in effector:target (E:T) ratio of 10:1, 5:1, and 1:1. The specific killing was assessed by flow cytometry. One representative experiment out of two to three independent experiments is shown. Symbols and error bars represent mean ± SEM of technical duplicates.

Back to article page