Shashi Singh, Peggy Paschke, Luke Tweedy and Robert Insall showed that the PKB and SKG kinases were involved in regulating the formation of cell projections and ultimately, the cells’ moving speed – mechanistically, the enzymes appeared to drive changes in the phosphorylation of the Scar/WAVE complex, which is a key driver for molecular changes at the front edge of a cell. [AKT and SGK kinases regulate cell migration by altering Scar/WAVE complex activation and Arp2/3 complex recruitment in Frontiers in Molecular Biosciences]

In Nature Communications, David Bryant, Eva Freckmann and Emma Sandilands with other Beatson scientists presented Traject3D – an imaging tool that allows the identification of distinct phenotypic patterns in 3D, live cell culture over time. This can give insights, for example, into how cellular phenotypes change with treatment exposure or how drugs can be combined to target resistant cell populations.

Deploying extensive transcriptional profiling methodologies, researchers led by Dr Philip Dunne described a disconnect in gene expression signatures between preclinical and clinical samples of colorectal cancer. Tumour models often do not accurately represent the stromal compartment and the immune microenvironment, which therefore might lead to the misinterpretation of mechanistic signalling relevant to the clinic. [Biological Misinterpretation of Transcriptional Signatures in Tumor Samples Can Unknowingly Undermine Mechanistic Understanding and Faithful Alignment with Preclinical Data in Clinical Cancer Research]

In their study, Aldo Bader, Martin Bushell and colleagues showed that the RNA helicase DDX17 was required for efficient DNA double strand break repair. At damage sites, DDX17 is key for RNA:DNA hybrid formation – an essential for effective repair – especially at genomic locations where RNA:DNA hybrids have failed to form.