Research in our lab is aiming to discover:

Mechanisms of resilience against age-related conditions

We discovered that a genetic alteration affecting the regulation of the transcription factor C/EBPβ by the nutrient and energy signalling pathway mTORC1 dramatically improves metabolic health, frailty and lifespan in mice. The same mutation also protects against unfavourable fat storage in response to a high-energy diet. Altogether our studies point to a pivotal role of C/EBPβ in fat metabolism and ageing. How these two mechanisms are connected is subject of current study as well as we seek to translate our findings into clinical applications.

Oncogenic functions of C/EBPs

Aberrantly high expression of the C/EBPβ-LIP transcription factor has several oncogenic functions in triple-negative breast cancer. In particular, the oncogenic mechanisms of C/EBPβ-LIP upregulation are unknown. Studies investigating the oncogenic functions of C/EBPβ-LIP suggest a key role in cancer cell migration and immune evasion. Both are subject of current investigations in our lab.

Tumour-suppressive functions of the TSC-mTORC1 pathway

Activation of the nutrient and energy sensitive mTORC1 pathway has long been considered tumour promoting. Yet, we discovered that in certain cancer types mTORC1 activation is harmful for the cancer cell and that these cells have developed mechanisms to suppress mTORC1 involving the tuberous sclerosis complex (TSC). Current research is investigating the underlying mechanisms and cellular changes that cause cancer cell death. In addition, we seek to develop drug screening strategies to target TSC and induce cancer cell death as a therapeutic option.