Publication Highlights: March & April 2022
Vasileios Papalazarou, James Drew and Beatson colleagues made a pre-print available that lends further evidence towards the idea that cancer cell behaviour can be influenced by sensing mechanical cues from the environment. Notably, pancreatic cancer cells, in response to a softer culture substrate, reprogrammed their gene expression, releasing factors to alter their own surroundings. In particular, the scientists found that the upregulation of collagen-VI and changes to the extracellular matrix ultimately encouraged the migration and invasion of these cells.
In their article in Developmental Cell, Kai Cao, Joel Riley and co-authors reported a link between impaired mitochondrial function and DNA damage. Dysfunctional, fragmented mitochondria engaged in a process called minority MOMP that triggers the activity of caspases which in turn leads to oncogenic DNA damage. They also suggested mechanisms by which a protein called BCL-2 could be targeted to prevent these cancer promoting signals.
In a multi-omics approach in iScience, Mark Salji, Hing Leung and others uncovered targetable pathways in models of castration-resistant prostate cancer (CRPC). Untargeted metabolomics revealed an accumulation of NAA and NAAG across different models of CRPC. Although additional work is required to evaluate the highlighted pathways, this study demonstrated the feasibility of a multi-omics approach for providing a data-rich resource for cancer research.
A study published in Cell Death & Differentiation by Tim Humpton together with Beatson scientists described a role for p53 in supporting the repair and recovery from acute liver damage. Through involvement of the detoxifying enzyme Cyp2a5/CYP2A6, p53 limited cell stress induced by reactive oxygen species and mediated regenerative processes – a function of p53 that also prevailed during chronic liver injury. As such, the authors suggested further investigation into Cyp2a5/CYP2A6 as a prognostic marker.