The molecular medicine research activity focuses on studying the links between clock factors and human pathologies, as well as on the identification and evaluation of novel molecules with “clock modulator” activity for therapeutic applications.

As an example, we recently discovered that the circadian regulator REV-ERBβ is over-expressed in several tumor cells and it operates as a cytoprotective factors upon genetic and pharmacological autophagy inhibition. As a consequence, REV-ERBβ inhibition induces apoptosis in cancer cells exposed to autophagy suppressor molecules, such as the clinically relevant drug, chloroquine.

In addition, we identified a novel class of dual REV-ERB/autophagy inhibitor compounds with a single-agent antitumor activity. This study is the first evidence that the pharmacological targeting of circadian regulators may be a suitable anticancer strategy.

We are now focused on the identification of the molecular connections between circadian signaling, autophagy and metabolism that support cancer cell viability.
Considering the increasing number of epidemiological evidences indicating an intimate link between circadian disruption and tumor development and progression, these studies will provide useful molecular and genetic insights on the circadian/cancer connection.


Our laboratory offers a vibrant research environment and opportunity to be involved in multidisciplinary research projects.
We provide comprehensive training for PhD students and postdoctoral fellows interested in a number of disciplines, including molecular genetics, biochemistry, physiology and pharmacology.


In collaboration with Prof. Ralf Paus (University of Manchester, UK), an expert in the field the biology and pathology of the skin, we also uncovered a molecular connection between the circadian clock and the human hair-follicle cycle, which has important clinical implications.

We further provided the first evidence that the molecular clock operates as a cell-autonomous modulator of human pigmentation, controlling the expression of key melanogenic genes through phosphorylation of the master regulator of melanogenesis, MITF.