TP53 is mutated in more than 50% of all human cancers, and the resulting mutant proteins often accumulate and acquire pro-oncogenic properties, “Gain-of-Function” (GOF), to drive tumourigenesis1 . Recent evidence demonstrated — targeting mutant p53 stabilization and tumour dependence on mutant p53 GOF as a promising approach for cancer treatment2 . In this study, we aim to identify novel regulators of mutant p53, decipher mechanism(s) underlying mutant p53 stabilization, and define their potential as therapeutic targets for cancer therapy.We performed genome-wide RNAi screens (protein-coding genes siRNA, microRNAs, long non-coding RNAs) on cancer cell-lines bearing endogenous mutant p53, and analyzed the mutant protein level and subcellular localization using high-content analysis. Candidate hits were triaged on secondary screens, and validated on multiple cancer cell-lines (tertiary screens). These candidate hits will be evaluated in vitro, for their effects on mutant p53 GOF and their roles underlying mutant p53 stabilization. Finally, the identified regulators — proteins, microRNAs and lncRNAs — will be analyzed-bioinformatically to better map the mutant p53 regulatory network.Our study has identified potential novel mutant p53 regulators (proteins, microRNAs and lncRNAs) to be further studied.
- Oren, M. and V. Rotter, Mutant p53 gain-of-function in cancer. Cold Spring Harb Perspect Biol, 2010. 2(2): p. a001107.
- Alexandrova, E.M., et al., Improving survival by exploiting tumour dependence on stabilized mutant p53 for treatment. Nature, 2015. 523(7560): p. 352-6.