Gruppo Rovida
Research Team’s name: Molecular Oncology & Cell Signalling
Coordinator: Elisabetta Rovida
Brief Biographical sketch of the Coordinator
Dr. Elisabetta Rovida obtained her Master’s degree in Biological Sciences cum laude from the University of Florence, Italy, in 1995. She earned her PhD in Experimental Pathology in 2001 at the same institution, under the supervision of Prof. Massimo Olivotto, carrying out part of her doctoral research at the University of Vienna (Austria) in the laboratory of Prof. Manuela Baccarini.
She subsequently completed ten years of postdoctoral training in basic cancer research at the University of Florence, including five years supported by fellowships from the Italian Association for Cancer Research (AIRC/FIRC), under the supervision of Dr. Persio Dello Sbarba. In 2011, she was appointed Assistant Professor at the Department of Experimental and Clinical Biomedical Sciences of the University of Florence.
Since 2015, Dr. Rovida has served as Principal Investigator or co-investigator in several research projects funded by national and international agencies. She acts as a reviewer for international scientific journals and funding bodies and is a member of multiple scientific societies.
Her research activity focuses on the role of kinases in cancer pathogenesis, with the aim of identifying therapeutic targets to reduce tumor growth and progression. In particular, her work concentrates on the Colony-Stimulating Factor 1 Receptor and mitogen-activated protein kinases, especially ERK5.
Dr. Rovida has authored more than 80 peer-reviewed scientific publications and numerous conference abstracts, primarily in the field of cancer biology. She has supervised undergraduate, graduate, and PhD students in Biological Sciences, Medical Biotechnologies, and Experimental and Clinical Oncology, and currently teaches General Pathology at the School of Medicine of the University of Florence.
Member of the Scientific Board the Doctorate/Phd Program in GENETICS, ONCOLOGY and CLINICAL MEDICINE (GenOMeC)Member of the following Scientific Societies: Società Italiana di Cancerologia (SIC); Società Italiana di Ematologia Sperimentale (SIES); Società Italiana di Patologia e Medicina Traslazionale (SIPMeT); European Association for Cancer Research (EACR).
Member of the editorial board of the following Journals: Topic Board member, International Journal of Molecular Sciences; Associate editor, Frontiers in Cell and Developmental Biology, section Signaling.
Research Team
Ignazia Tusa, staff scientist
Alessio Menconi, PostDoc
Ylenia Sfragano, PhD Student
Cosimo Mazzei, Post-graduate fellow
Serena De Gregorio, Post-graduate fellow
Current research interest
Identification of the molecular mechanisms responsible for sustained cell proliferation and reduced sensitivity to antiproliferative factors in tumor cells, with particular attention to the involvement in the aforementioned biological processes of the Colony-Stimulating Factor-1 Receptor (CSF-1R) and of the Mitogen-Activated Protein Kinases (MAPK), ERK5 in particular.
Identification of mechanisms of resistance to molecular therapies directed to MAPK in solid tumors and to BCR/ABL in chronic myeloid leukemia.
Key words
RTK, MAPK, hypoxia, targeted therapy, cancer, ERK5, CSF-1R, cellular senescence.
Current/recent sources of funding
2026-2031 (717634,50/5 years) Pincer attack on melanoma by targeting ERK5-related cellular senescence and nuclear translocation, funded by Associazione Italiana per la ricerca sul Cancro (AIRC). Role on project: Principal InvestigatorI.
2026-2027 (80000 €/2 years) “Identificazione dei trasportatori responsabili della traslocazione nucleare di ERK5 al fine di individuare nuove strategie terapeutiche contro il melanoma/Identification of transporters responsible for ERK5 nuclear translocation to identify new therapeutic strategies against melanoma”, funded by Fondazione Intesa Sanpaolo S.p.A. Role on project: Principal Investigator.
2024-2027 (57000 €/3 years) Co-funding of a PhD fellowship in Biomedical Sciences for the project “Identification of strategies aimed to inhibit ERK5 nuclear translocation for targeted therapy in cancer” PNRR (D.M. 118/2023)/NEXTGENERATIONEU. Role on project. Supervisor.
2025-2026 (89,000 €/2 years) Anti-alpha6 beta4 integrin antibodies in patients with mucous membrane pemphigoid: an European multicentric study, funded by the EADV: European Academy of Dermatology and Venereology. Role on project: Participant.
2023-2026 (96000 €/3 years) THE - TUSCANY HEALTH ECOSYSTEM funded by the Italian Mistry of the University and Research (https://www.mur.gov.it/sites/default/files/2022-06/22_06_28%20Scheda_ecosistema_Toscana_PNRR_MUR.pdf). Development and testing of new MEK5-ERK5 inhibitors to be exploited in the targeted-therapy of solid and liquid neoplasms subproject.Role on project: Unit leader.
2022-2024 (30000 € / 2 years) “Identification of the role of ERK5 in the onset of HBV- and HCV-induced hepatocellular carcinoma funded by Fondazione BENEFICENTIA Stiftung. Role on project: Principal Investigator.
2022-2024 (69600 € / 2 years) “Role of the protein kinase ERK5 in the pathogenesis of insulin resistance in the context of non-alcoholic steatohepatitis” funded by Università degli Studi di Firenze (Bando RTD). Call 2021. Role on project: Coordinator.
10 best pubblications of the last 5 years
1. Yang X, Yin W, Xu M, Tusa I, Menconi A, Dai Y, Ding Q, Wang G, Foley KP, Rovida E, Ying W. Development of a chaperone-mediated protein degrader targeting ERK5 that efficaciously reduces tumor growth. Cell Commun Signal. 2026 Feb 3. doi: 10.1186/s12964-026-02682-w.
2. Martella D, Tusa I, Tubita A, Negri A, Turriani M, Rojas-Rodríguez M, de Luna MS, Menconi A, Parmeggiani C, Rovida E. Liquid Crystalline Networks Hamper the Malignancy of Cancer Cells. Adv Healthc Mater. 2025 14(7):e2403607. doi: 10.1002/adhm.202403607.
3. Lombardi Z, Gardini L, Kashchuk AV, Menconi A, Lulli M, Tusa I, Tubita A, Maresca L, Stecca B, Capitanio M, Rovida E. Importin subunit beta-1 mediates ERK5 nuclear translocation, and its inhibition synergizes with ERK5 kinase inhibitors in reducing cancer cell proliferation. Mol Oncol. 2025 19(1):99-113. doi: 10.1002/1878-0261.13674.
4. Tusa I, Menconi A, Tubita A, Rovida E. Pathophysiological impact of the MEK5/ERK5 pathway in oxidative stress. Cells 2023, 12, 1154. doi: 10.3390/cells12081154.
5. Maglie R, De Almeida CV, Baffa ME, Bianchi B, Caproni M, Di Zenzo G, Li X, Hirako Y, Hashimoto T, Tusa I, Lulli M, Rovida E§, Antiga E. Anti-β4 integrin autoantibodies in patients with mucous membrane pemphigoid: a retrospective analysis from a tertiary centre in Italy. J Eur Acad Dermatol Venereol. 2023 37(2):e249-e251. doi: 10.1111/jdv.18617.
6. Franci L, Tubita A, Bertolino FM, Palma A, Cannino G, Settembre C, Rasola A, Rovida E, Chiariello M. MAPK15 protects from oxidative stress-dependent cellular senescence by inducing the mitophagic process. Aging Cell. 2022 21(7):e13620. doi: 10.1111/acel.13620.
7. Tubita A, Lombardi Z, Tusa I, Lazzeretti A, Sgrignani G, Papini D, Menconi A, Gagliardi S, Lulli M, Dello Sbarba P, Esparís-Ogando A, Pandiella A, Stecca B, Rovida E. Inhibition of ERK5 elicits cellular senescence in melanoma via the cyclin-dependent kinase inhibitor p21. Cancer Res. 2022 82(3):447-457. doi: 10.1158/0008-5472.CAN-21-0993.
8. Tusa I, Gagliardi S, Tubita A, Pandolfi S, Menconi A, Lulli M, Dello Sbarba P, Stecca B, Rovida E. The Hedgehog-GLI pathway regulates MEK5-ERK5 expression and activation in melanoma cells. Int. J. Mol. Sci. 2021 22(20):11259. doi: 10.3390/ijms222011259.
9. Gentilini A¶, Lori G, Caligiuri A, Raggi C, Di Maira G, Pastore M, Piombanti B, Lottini T, Arcangeli A, Madiai S, Navari N, Banales JM, Di Matteo S, Alvaro D, Duwe L, Andersen JB, Tubita A, Tusa I, Di Tommaso L, Campani C, Rovida E§, Marra F. ¶Extracellular signal-regulated kinase 5 regulates the malignant phenotype of cholangiocarcinoma cells. Hepatology 2021 74(4):2007-2020. doi: 10.1002/hep.31888.
10. Tubita A, Tusa I, Rovida E. Playing the Whack-a-mole Game: ERK5 Activation Emerges among the Resistance Mechanisms to RAF-MEK1/2-ERK1/2-targeted Therapy. Front. Cell Dev. Biol., 2021 Mar 11;9:647311. doi: 10.3389/fcell.2021.647311.
Main scientific contributions
Demonstration that ERK5 is a key signalling kinase in the pathogenesis of liver cancers and melanoma. Spanning from studies that identified a key role of ERK5 in the proliferation of cells that are important for chronic inflammation and thus for cancer onset and progression (Rovida et al, J Hepatol 2008; Rovida et al, J Immunol, 2008; Seidita et al, and Rovida and Donati FASEB J 2023), ER recently showed that ERK5 is a key regulator of the growth of hepatocellular carcinoma (Rovida et al, Gut 2015), cholangiocarcinoma (Gentilini et al, and Rovida and Marra Hepatol 2021) and melanoma (Tusa et al, and Rovida, Oncogene 2018; Tusa et al, and Rovida Int. J. Mol. Sci. 2021) cells in vitro and in vivo. A recent study by ER’s group showed, for the first time, the existence of a link between ERK5 inhibition and the occurrence of cellular senescence (Tubita et al, and Rovida Canc Res 2022).
Advancement of the knowledge of the relevance of ERK5 in the biology of cancer and as a target for cancer therapy (Rovida & Stecca, Semin Cancer Biol. 2015; Stecca & Rovida Int J Mol Sci. 2019; Tubita et al, and Rovida Int J Mol Sci. 2020; Tubita et al, and Rovida. Front Cell Dev Biol. 2021; Tusa et al, and Rovida. Cells 2023).
Identification of the protease responsible for CSF-1R cleavage and establishment of a relevant role and a new mechanism of action of the Colony-Stimulating factor Receptor in breast cancer cells.
The hematopoietic colony-stimulating factor 1 (hCSF-1) is essential for innate and adaptive immunity against viral and microbial infections and cancer. ER identified the TNF alpha converting enzyme (TACE, also called ADAM17) as the protease responsible for the cleavage of its receptor CSF-1R (Rovida et al, J Immunol 2001). This finding is very important in light of the fact that TACE is a potential target for cancer therapy and that CSF-1R is responsible for macrophage proliferation and survival as well as for the proliferation of several neoplastic cells. In breast cancer cells, ER described a relevant role of the Colony-Stimulating factor Receptor (CSF1R) (Morandi et al, PlosOne 2011) and identified a new mechanism of CSF-1R action which involves CSF-1R translocation into the nucleus and its binding to the promoter of proliferation-related genes in breast cancer cells (Barbetti et al, Oncogene 2013; Rovida and Dello Sbarba, In J Mol Sci 2014).
Discovery of a new mechanism of resistance to Imatinib in chronic myeloid stem cells and identification of BCR/ABL-unrelated targets useful for targeting TKi-insensitive CML stem cells. We found that hypoxia, a condition that normally occurs in the hematopoietic stem cell niche, suppresses the BCR/Abl oncogenic protein, so that Chronic Myeloid Leukaemia (CML) stem cells (LSC) are completely insensitive to the BCR/Abl inhibitor imatinib mesylate (IM), the main drug currently used for CML therapy (Giuntoli et al, Leukemia 2006). Along this line, studies conducted under the supervision of ER identified pharmacological treatments (i.e. hypoxia-inducible factor inhibitor acriflavine and ERK5 inhibitors) that are active on TKI-insensitive CML progenitor/stem cells (Cheloni et al, Blood 2017; Tusa et al, and Rovida, Dello Sbarba Stem Cell Reports 2018).
Identification of an anti-leukemic effect of histone deacetylase inhibitors in acute myeloid leukaemia.
13. Collaborations
Atanasio Pandiella, Instituto de Biología Molecular y Celular del Cáncer (IBMCC), Salamanca Spain.
Rony Seger, Department of Immunology & Regenerative Biology, Weizmann Institute of Science, Rehovot, Israel.
Nathanael Gray, Dana-Farber Cancer Institute, Harvard Medical School, Boston, USA.
Azucena Esparis-Ogando, Instituto de Biología Molecular y Celular del Cáncer (IBMCC), Salamanca Spain.
Manuela Baccarini, Center for Molecular Biology, Max F. Perutz Laboratories, University of Vienna, Vienna, Austria.
Barbara Stecca, Istituto per lo Studio e la Prevenzione e la Rete Oncologica (ISPRO), Florence, Italy.
Cathy Tournier, University of Manchester, Michael Smith Building, Manchester, United Kingdom.
Fabio Marra, Dipartimento di Medicina Sperimentale e Clinica Università di Firenze, Florence, Italy.
Antonella Gozzini, Unità Funzionale di Ematologia, Azienda Ospedaliro-Universitaria Careggi (AOUC), Florence, Italy
Sandra Donnini, Dipartimento di Scienze della Vita, Università di Siena, Italy.
Shaoguang Li, Aaron Lazare Medical Research Building (LRB), UMass Medical School, Worcester, MA, USA.
Ultimo aggiornamento
13.04.2026