Fig. 2

Schematic showing p53 role in cancer stemness. a. Wildtype p53 can modulate the expression of stem cell transcription factors to control pluripotency. Nanog can suppress p53 activity by activating Mdm2 to promote pluripotency. b. Mutant p53 can activate the CSC markers such as ALDHA1, CD44, and LGR5 by binding to their promoters to promote stemness. By upregulating the anti-apoptotic genes Bcl-2 and the multidrug resistance gene MDR1, mutant p53 can encourage the characteristic CSC phenotype of increased drug resistance and prolonged survival. Mutant p53 regulates c-Myc and can increase the expression of miR-324-5p resulting in the downregulation of CUEDC2, a miR-324-5p downstream target gene, which activates NF-kB pathway exhibiting cancer stemness features. c. Amyloid p53 can upregulate LIF and STAT3 probably contributing to the cancer stemness phenotype