Fig. 3
From: p53: from understanding its structure to advances in therapeutic targeting
p53 can regulate the tumor immune microenvironment to suppress tumorigenesis. a The tumor immune microenvironment associated with wild-type p53 plays an antitumor role. Wild-type p53 can increase the expression levels of miR34a and UL16-binding protein 1/2 (ULBP1/2). miR34a reduces PDL1 expression levels through inhibiting PDL1 mRNA translation and promoting PDL1 degradation, which enhances CD8+ T-cell-mediated killing. ULBP1/2, as activating ligands of natural killer (NK) cells, can enhance the cytotoxicity of NK cells. Conversely, wild-type p53 expression can promote the secretion of antitumor cytokines to inhibit tumorigenesis. b In TP53-mutated cells, downregulation of miR34a and ULBP1/2 expression decreases the killing ability of CD8+ T cells and NK cells. Mutated p53 proteins promote the secretion of exosomes that transform M1 macrophages (antitumor cells) into M2 macrophages (protumor cells) by delivering microRNAs such as miR-1246. In addition, cytokines secreted by protumor cells can attenuate the antitumor response. This figure was created by BioRender.com
