Our research focuses on the molecular mechanisms controlling the growth, differentation and migration of cancer cells.1. The first line of research is focused on the characterization of signalling pathways and posttranslational modifications that control the abundance of cell cycle regulatory proteins. We study how dysregulation of these processes leads to accelerated cell growth and allow adaptation of the cancer cells to their environment.2. The second line of research is focused on translational research of lung cancer stem cells (CSCs). CSCs have the capacity to self-renew, differentiate, initiate and maintain the tumor growth. In addition, these cells are resistant to conventional chemotherapy. Therefore CSCs are a promising therapeutic target with great potential. Our goal is to develop personalized treatment strategies that will minimize the evolution of lung tumors to the current treatment.

Regulation and function of AP-1 transcription complex in cancer cells. AP-1 transcription factors are crucial molecules for integrating intra-and extracellular signals, and their activity is regulated by a series of post-translational modifications. AP-1 is also involved in various pathologies, including cancer in which AP-1 proteins are often dysregulated. In this context, I investigated the molecular mechanisms that control AP-1 metabolic protein turnover and how the stabilization and accumulation of AP-1 contribute to cell growth and proliferation.

The ProteoCure COST Action aims at fostering research and innovation in the field of proteolysis with the goal of manipulating the proteolysis machinery for the development of novel, specific and efficient therapies.Proteins are essential molecular actors in every cellular process. From their synthesis to their degradation, they are subject to continuous and precise quality control mechanisms to ensure that they properly and timely take on their functions to fulfil cellular needs.

Regulation and function of JunB transcription factor in cancer cells. I investigated the molecular mechanisms by which dysregulation of JunB, a member of the AP-1 transcription factor family, alters gene expression and cell cycle progression in cancer cells. In addition to studies of ubiquitylation and proteasomal degradation of JunB, I also pursued the characterization of its bona fide genomic targets combining large-scale genomic and transcriptomic approaches with functional studies.

Regulation of stress, hormone and metabolic responses by SnRK1 kinases and the Ubiquitin-Proteasome System.SnRK1 kinases play a central role in controlling key metabolic enzymes and transcription in response to glucose availability and changes in cellular energy homeostasis. I Investigated the interaction of SnRK1 kinase with the SCF (SKP1-CULLIN1-F-box protein) E3 ubiquitin ligase