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. 2021 Jun 23;2:676643. doi: 10.3389/froh.2021.676643

Figure 1.

Figure 1

Two strategies to combat therapy-resistance caused by mutant TP53 proteins in HPV(-) HNSCC. Mutant, gain-of-function (GOF) TP53 loses the function of WT TP53 (e.g., cell cycle arrest, DNA repair, apoptosis) and acquires tumor proliferation and metastasis functions (black lines). PRIMA-1 and PRIMA-1-met bind to mutant TP53, interact with the DNA-binding domain, and restore WT TP53 functions (blue lines). Inhibition of HSP90 chaperone machinery destabilizes GOF TP53, which leads to cell death (orange lines).