PRIVES LABORATORY
Metabolism, invasion and therapeutic vulnerabilities

Research programme 04

Metabolism, invasion and therapeutic vulnerabilities

We trace how p53 status rewires the mevalonate pathway, cytoskeletal signalling and tumour invasion to identify mutation-selective treatment opportunities.

Central question

Can metabolic and signalling dependencies created by mutant p53 be exploited without compromising wild-type p53 tumour suppression?

Wild-type and mutant p53 can exert opposing effects on metabolic pathways. Work from the laboratory has linked p53 to the mevalonate pathway, a biosynthetic system that supports membrane production, protein prenylation and oncogenic signalling.

Current studies connect this pathway with Rho/ROCK-dependent invasion in complex environments and test whether pathway inhibition can destabilise mutant p53 or suppress its downstream phenotypes.

Confocal and organoid microscopy showing mutant-p53 tumour morphology and invasion after therapeutic perturbation. Figure 4, Oncogene (2017). Reused unchanged under CC BY 4.0.
Confocal and organoid microscopy showing mutant-p53 tumour morphology and invasion after therapeutic perturbation. Figure 4, Oncogene (2017). Reused unchanged under CC BY 4.0.
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