Mon 28-06-2021 15:10 PM
ABU DHABI, 28th June, 2021 (WAM) -- A new study by an international team of researchers, led by NYU Abu Dhabi Associate Professor of Biology Mazin Magzoub, provides important insights into the p53 protein, a critical tumour suppressor often mutated and deactivated in cancer and a key target in the development of cancer therapeutics.
In the paper titled "Protein mimetic amyloid inhibitor potently abrogates cancer-associated mutant p53 aggregation and restores tumour suppressor function," published in the journal Nature Communications, researchers in the Magzoub Lab, along with colleagues at NYUAD, presented the process of using protein mimetics to reactivate p53.
The team first screened a library of protein mimetics originally designed to target Alzheimer’s disease and type II diabetes. The screen identified a protein mimetic that potently dissociates mutant p53 aggregates and prevents further aggregation of the protein. The researchers then demonstrated that dissociation of mutant p53 aggregates by the protein mimetic restores p53’s tumour suppressor function, leading to the death of a wide range of cancer cells.
Importantly, treatment with the protein mimetic effectively shrinks tumours that harbour mutant p53, while exhibiting no noticeable toxicity to healthy tissue, thereby substantially prolonging survival.
"With the increasing incidence of cancer worldwide, there is a pressing need for new cancer treatments to supplement or supplant the current ones," said Magzoub.
"Here, we have demonstrated the first successful application of a bona fide small-molecule amyloid inhibitor as an anticancer agent. We believe this work will have a broad impact as it effectively establishes a bridge between amyloid diseases and cancer, providing a foundation for cross-informational approaches in the design of new and potent mutant p53-targeted cancer therapeutics."