TP53, often called the “”guardian of the genome””, protects cells from cancer by instructing damaged cells to undergo cell-cycle arrest, DNA repair, or programmed cell death. Of note, TP53 activation can produce different cellular outcomes depending on cellular context. Although all above mentioned processes can suppress the development and expansion of cancers, cell death is the most desirable therapeutic outcome as it eliminates cancer cells, whereas cell-cycle arrest may allow tumour cells to persist and potentially resume proliferation.
This project aims to define the TP53 protein interaction network in cancer cells that exhibit distinct outcomes after TP53 activation. Using cutting-edge proteomics, we will determine whether differences in TP53-associated protein complexes contribute to divergent cell fate decisions, with the goal to identify therapeutic targets that may be exploited to induce the killing of cancer cells.