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. Author manuscript; available in PMC: 2020 Feb 19.
Published in final edited form as: Oncogene. 2019 Aug 19;38(49):7433–7446. doi: 10.1038/s41388-019-0960-x

Fig. 2. Inhibition of the NF-κB pathway abolished CD8+ T cell–mediated NKG2D ligand upregulation.

Fig. 2.

CT26 (A) and K7M3 (B) cells were pretreated with an NF-κB pathway inhibitor: STAT inhibitor S3I-201 (50 μM for 24 h), p38 inhibitor PH797804 (1 μM for 4 h), MAPK kinase (MEK) inhibitor PD98059 (2 μM for 4 h), PI3K inhibitor PKI-587 (5 nM for 4 h), or NF-κB inhibitor QNZ (100 nM for 4 h). The pretreated cells were then labeled with CFSE and cultured in the presence or absence of stimulated mouse CD8+ T cells (1:1 tumor cell-to-T cell ratio). Rae-1 expression on the tumor cell surface was determined via flow cytometry. iso ctrl: isotype control. Bar graphs show means ± SEM. Results are representative of three repeated experiments. ** P<0.01; **** P<0.001; ns, no statistical significance