TP53 (also called TRP53 or p53, used hereafter), is one of the most important tumour suppressors in our cells. When activated, p53 can stop cells from proliferating, or it can trigger them to die by undergoing apoptosis. But why do some cells die while others survive and enter a long-lasting state of proliferation arrest known as senescence? This fundamental question has important implications for developing more effective treatments for cancer patients.
His research has revealed that the fate of a cell after p53 activation is influenced not only by the genes switched on by p53, but also by the cell’s pre-existing molecular state. By combining RNA sequencing, proteomics and functional experiments across a diverse range of non-transformed cell types, his research identified features of cells that help determine whether they will survive and undergo proliferation arrest or undergo apoptosis following p53 activation. These findings have also led to the development of a computational model that can predict whether cancer cells will survive and stop proliferation or undergo apoptotic death after p53 activation. In the future, this work could contribute to more personalised approaches to cancer
Dr Shuai Huang is a Senior Research Officer in the Cancer Division. He completed his PhD at WEHI in 2021 under the supervision of Professor Grant Dewson, Dr Mark van Delft and Professor David Huang, where he identified the E3 ubiquitin ligase MARCH5 as a novel regulator of the intrinsic apoptosis pathway. He subsequently joined the laboratories of Professor Andreas Strasser and Prof Gemma Kelly, where his research has focused on understanding why p53 induces different cellular outcomes in different types of cells and how these responses can be manipulated to improve cancer treatment.