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Ferruccio Galbiati, PhD

Professor & Vice Chair for Research
E1154 Thomas E. Starzl Biomedical Science Tower
Pittsburgh, PA 15261
Phone: 412-648-2047
Fax: 412-648-1945


BS (Biology), University of Milan, Italy, 1992
PhD (Biology), University of Milan, Italy, 1996
Postdoctoral Fellow, Department of Molecular Pharmacology, Albert Einstein College of Medicine, 2000
Headshot of Ferruccio Galbiati, PhD
Most cells cannot divide indefinitely due to a process termed cellular senescence. Because cancer cells need to escape cellular senescence in order to proliferate and eventually form tumors, it is well accepted that cellular senescence is a powerful tumor suppressive mechanism. In addition, since several molecular changes that are observed in senescent cells occur in somatic cells during the aging process, investigating the molecular mechanisms underlying cellular senescence will also provide a better understanding of the more complicated aging process. Thus, molecules that regulate cellular senescence represent potential therapeutic targets for the prevention/treatment of cancer as well as the fight against aging.
Our work is directed at unraveling the role of caveolin-1 as a novel mediator of cellular senescence. Caveolin-1 is the structural protein component of caveolae, invaginations of the plasma membrane involved in signal transduction. Caveolin-1 acts as a scaffolding protein to concentrate, organize, and functionally modulate signaling molecules within caveolar membranes.
Our laboratory was the first to demonstrate that caveolin-1 plays a pivotal role in oxidative stress-induced premature senescence. We found that oxidative stress upregulates caveolin-1 protein expression through the p38 MAPK/Sp1-mediated activation of the caveolin-1 gene promoter. We also demonstrated that caveolin-1 promotes premature senescence through activation of the p53/p21Waf1/Cip1 pathway by acting as a regulator of Mdm2, PP2A-C, TrxR1, Nrf2 and Sirt1. More recently, we have shown that caveolin-1 promotes oncogene-induced senescence in cells and a mouse model of lung cancer.
Taken together, our findings indicate that caveolin-1 plays a central role in the signaling events that lead to cellular senescence. Our current main research interest is the identification, at the molecular level, of novel signaling pathways that link caveolin-1 to premature senescence and their relevance to aging and age-related diseases, such as cancer, using both cellular and animal models. These investigations will provide novel insights into cellular and molecular mechanisms underlying aging and cancerous cell transformation and will identify novel molecular targets that can be exploited for the development of alternative therapeutic options toward age-related diseases, including cancer.







Journal Articles

Jeffries EP, M Di Filippo and F Galbiati. Failure to reabsorb the primary cilium induces cellular senescence. FASEB J 33:4866-4882, 2019.
Volonte D, AR Vyas, C Chen, S Dacic, LP Stabile, BF Kurland, SR Abberbock, TF Burns, JM Herman, YP Di and  F Galbiati. Caveolin-1 promotes the tumor suppressor properties of oncogene-induced cellular senescence. J Biol Chem 293:1794-1809, 2018.

Volonte D, Zou H, Bartholomew JN, Liu Z, Morel PA and Galbiati F. Oxidative stress-induced inhibition of Sirt1 by caveolin-1 promotes p53-dependent premature senescence and stimulates the secretion of IL-6. J Biol Chem 290:4202-4214, 2015.

Volonte D, Z Liu, PM Musille, E Stoppani, N Wakabayashi, YP Di, MP Lisanti, TW Kensler and F Galbiati.  Inhibition of nuclear factor-erythroid 2-related factor (Nrf2) by caveolin-1 promotes stress-induced premature senescence.  Mol Biol Cell 24:1852-1862, 2013.
Zou H, D Volonte and F Galbiati.  Interaction of caveolin-1 with Ku70 inhibits Bax-mediated apoptosis.  PLoS One 7:e39379, 2012.
Volonte D and F Galbiati.  Polymerase I and transcript release factor (PTRF)/cavin-1 is a novel regulator of stress-induced premature senescence.  J Biol Chem 286:28657-28661, 2011.

Hezel M, de Groat WC and Galbiati F.  Caveolin-3 promotes nicotinic acetylcholine receptor clustering and regulates neuromuscular junction activity. Mol Biol Cel 21: 302-310, 2010.

Bartholomew JN, D Volonte and F Galbiati. Caveolin-1 regulates the antagonistic pleiotropic properties of cellular senescence through a novel Mdm2/p53-mediated pathway. Cancer Research 69:2878-2886, 2009.
Volonte D, B Kahkonen, S Shapiro, Y Di and F Galbiati. Caveolin-1 expression is required for the development of pulmonary emphysema through activation of the ATM-p53-p21 pathway. J Biol Chem 284:5462-5466, 2009.
Volonte D and F Galbiati. Inhibition of thioredoxin reductase 1 by caveolin-1 promotes stress-induced premature senescence. EMBO Reports 10:1334-1340, 2009.

Sponsored Research

Mechanisms that control the progression from premalignant lesions to adenocarcinomas in the lung - 4/1/2017 - 3/31/2022
NIH - R01CA205165