PhD in CELLULAR AND MOLECULAR BIOLOGY

email: filomeni@bio.uniroma2.it
phone: 06 7259 2215
building: SOGENE
room: 215

Education and training

1999-2002 Ph.D. in Cellular and Molecular Biology, Tor Vergata University, Rome

1997 MSc cum laude, Tor Vergata University, Rome

Employment

2022- Associate Professor of Biochemisrty, Tor Vergata University, Rome (IT).

2013- Group Leader, Danish Cancer Institute, Copenhagen, Denmark (DK).

2010-2013 Young Group Leader, Research Center IRCCS San Raffaele Pisana, Rome, (IT).

2007-2022 Researcher, Tor Vergata University, Rome (IT).

2004-2007 Talented Young Researcher, “Funding for Base Research Investments” of the Ministry of University and Research (FIRB – MIUR), Tor Vergata University, Rome (IT).

Teaching

2013- Biochemistry – MD in Bioinformatics. Tor Vergata University, Rome.

2007-2013 Redox Signaling and Cellular Stress – MD in Cellular and Molecular Biology, and Human Biology. Tor Vergata University, Rome.

2011-2013 Physic world, Macromolecules and Life, – MD in Cellular and Molecular Biology, and Human Biology. Tor Vergata University, Rome.

2011 Nutraceuticals and Carcinogenesis, – MD in Cellular and Molecular Biology. Tor Vergata University, Rome.

Honors and International Commitments

2023: Nominated for the Society for Free Radical Research – Europe Council

2023: Organizer and Chair of the Symposium titled Cancer Metabolism Snapshot at the Danish Cancer Institute: New Insights and Therapeutic Perspectives (Copenhagen, Denmark, 26 Oct)

2023: Organizer and Chair of the Symposium titled Biophysics of Redox Biology: Methods, Insights, and Novel Opportunities within the Annual Meeting of the European Biophysical Societies' Association – EBSA (Stockholm, Sweden, 31 Aug-4 Sept)

2023: Organizer and Chair of the Symposium titled Redox Regulation of Phosphorylation: Effects on Translation and Translational Opportunities, the Annual Meeting of SFRR-E (Vienna, Austria, 6-9 Jun)

2022: VIII Workshop on Nitric Oxide in Cancer – Special Focus: Metabolism and Aging (Copenhagen, Denmark, 8-10 Jun)

2019: Organizer and Chair of the Symposium titled Redox and Metabolic Signaling in Cancer within the Annual Meeting of SFRR-E (Ferrara, Italy, 19-21 Jun)

2019-2024 Affiliated Researcher of the Center for Healthy Aging, University of Copenhagen

2018-: Member of the Research Leader Council, Danish Cancer Institute

2017- Founder Member of the International Society for Nitric Oxide in Cancer (ISNOC)

2014- Member of the Society for Free Radical Research – Europe (SFRR-E)

2013-2024 Member of the Center of Excellence in Autophagy, Recycling and Disease

2004 Young Investigator Award, Society for Free Radical Research-Europe Lodz (Poland).

Research Interests

The main value of my research is to combine knowledge of cancer metabolism and redox signaling with state-of-the-art technology. By means of such a synergy, in the last few years, my team focused on S-nitrosylation (SNO), the reversible modification of cysteine residues by nitric oxide (NO), and discovered that conditions of deregulated SNO, such as those resulting from deficiency in the denitrosylating enzymes, correlate with aging, cancer, and human diseases. We discovered that SNO deeply affects myoblast differentiation (Cell Death Dis., 2019) and skeletal muscle physiology (Antiox. Redox Signal., 2014). The alteration of these processes is associated with the selective SNO of proteins controlling mitochondrial dynamics and quality control and play a driving role in cell senescence and mammalian aging (Proc. Natl. Acad. Sci., 2018). By affecting mitochondrial dynamics and mitophagy, we found that SNO indirectly modulates intracellular reactive oxygen species (ROS) production and oxidative stress. This provides further support for the hypothesis that uncontrolled and aberrant SNO plays a role in aging and acts as a driver process in the development of cancer (Cancer Res., 2016; Cell Rep., 2023). Along this line, we recently discovered that the denitrosylating capacity of a cell is functionally linked to the oncopATM (ataxia telangiectasia mutated) and required to modulate ROS production from burned-out mitochondira and increase cell tolerance to oxidative stress (EMBO Rep., 2020).