Fig. 3

MDM2 can induce the immune evasion of tumor cells. In tumor cells, MDM2 is known to increase the degradation of P53, which consequently results in a decline in the levels of natural killer cell-activating receptors (NK-ARs) and NK-mediated killing. Additionally, MDM2 in these cells can directly impede CD4 + T cells, as well as the production of interleukin-2 (IL-2) and interferon-γ (IFN-γ). Furthermore, MDM2 in CD4 + T cells hinders NFATc2 expression, thereby suppressing the activation of these cells. However, MDM2 in CD8 + T cells can actually stabilize STAT5 and boost their activation. Despite this, APG-115 presents an effective opportunity to upregulate both P53 and MDM2 and thereby enhance the anticancer immunity induced by CD8 + T cells. The figure also demonstrates the effectiveness of MDM2 inhibitors in inhibiting immune evasion induced by MDM2