Skip to main content
European Commission logo print header

P53-dependent Metabolic and Epigenetic Reprogramming in Carcinogenesis

Project description

A guardian angel turned devilish could reveal therapeutic targets for many cancers

Cancer is diverse and complex but many cancers show certain similarities. Mutations in the TP53 gene coding tumour protein 53 (p53) are most commonly associated with human cancers. As the 'guardian of the genome', p53 regulates cell division and acts as a tumour suppressor, stopping cells with mutated or damaged DNA from dividing. In addition, TP53 mutation alters cell metabolism, which in turn, can affect modifications to DNA that control gene expression (epigenetics), resulting in abnormal gene expression that further promotes cancer development. MetEpiC is investigating this cycle of interactions for a clearer understanding of pathways with implications for therapeutically targeting several types of cancers.


Carcinogenesis is a multi-factorial disease which combines genetic mutations, aberrant epigenetic landscape and altered cell metabolism. TP53 which is the most mutated gene in human cancers, is known to regulate cell metabolism. It has been recently established that the metabolic status of cells can modulate the epigenetic landscape. The goal of this proposal is to characterize metabolic-driven modulation of epigenetic landscape during carcinogenesis using TP53 mutated cancers as models. In this project, we plan to address how TP53 mutations alter cell metabolism and the epigenome, thus creating abnormal gene expression facilitating carcinogenesis. Thanks to our preliminary data we will focus our attention on Acetyl-CoA metabolism and histone acetylations. This project will take advantage of state-of-the art approaches such as metabolomics, epigenomics and transcriptomics. My expertise on epigenetics and metabolism, as well as the expertise of the supervisor in the field of TP53 and carcinogenesis, are major assets for this project. Altogether, we expect that unraveling novel mechanisms interconnecting TP53 mutations, cellular metabolism and epigenome will provide new insights for understanding cancer development. Moreover, we expect to propose innovative strategies to tackle cancers harboring mutated TP53 thanks to combination of drugs targeting metabolism and the epigenome. This fellowship will definitively help me to conduct a unique and promising research line in the European Community with the final goal to establish myself as an independent scientist.


Net EU contribution
€ 196 707,84
Other funding
€ 0,00