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. 2024 Jan 25;51(1):205. doi: 10.1007/s11033-023-09097-7

Fig. 3.

Fig. 3

Schematic diagram of tumor cells lacking WT p53 or expressing Mut p53 against NK cell killing. WT p53 can directly up-regulate the expression levels of ULBP1 and ULBP2, members of the ligand family of NKG2D on the surface of tumor cells and enhance the anti-tumor immune response mediated by NK cells. JQ1, a BET-bromine domain inhibitor of oncogene MYCN, can down-regulate the levels of c-MYC and p53, and then down-regulate the expression of NKG2DL, making tumor cells resistant to NK cell-mediated killing. Dichloroacetate (DCA), a glycolytic inhibitor, can also down-regulate the expression of MICA, MICB and ULBP-1 of NKG2DL family in tumor cells lacking WT p53 or expressing Mut p53, thus mediating immune escape