Massimo Zollo
Massimo Zollo
affiliation: Università di Napoli Federico II
research area(s): Computational Biology
Course: Computational Biology and Bioinformatics
University/Istitution: Università di Napoli Federico II
1989 University "Federico II" Naples, Italy Degree in Biological Sciences "Cum Laude". Field of study: Biological Sciences "Genetics"
1985 International Institute of Genetic and Biophysical CNR - Residency. Field of study: Human Genetics

Research Interests:Human Genetics, Molecular Biology and Oncology, Functional Genomics and Biotechnology
Research and Professional Experience:
1986-1989: Research Fellow at the International Institute of Genetics and Biophysics (IIGB), CNR, Naples, Italy.
03/89-09/89: Postdoctoral Fellow at the National Institute of Health, NIDDK department, Bethesda (National Institute of Health.), MD. , USA.
1989-1991: Postdoctoral Fellow at the International Institute of Genetics and Biophysics (IIGB), CNR, Naples, Italy.
1991: Postdoctoral Fellow (Research Associate) at the Washington University, St. Louis, Missouri, USA.
07/91-01/92: Visiting Scientist Genentech Inc., South San Francisco, CA, USA.
02/92: Visiting Scientist at the Department of Advanced Center for Genetic and Technology, Applied Biosystems, Foster City, CA, USA.
02/93: Associate Scientist at Applied Biosystems, California, USA.
04/94: Product DNA Specialist and Group Leader at Life Science Technology, Perkin-Elmer-Applied Biosystems, Monza, Italy.
01/95: Coordinator of the Sequencing Core Laboratory at TIGEM, Telethon Institute of Genetics and Medicine, Milan, Italy.
2000-2005: Staff Scientist and researcher at TIGEM, Telethon Institute of Genetics and Medicine, Naples, Italy
Coordinator TIGEM-IIGB Sequencing Core, TIGEM, Telethon Institute of Genetics and Medicine, Naples, Italy
2001: Member of the teaching staff: Doctorate in Molecular Oncology and Pharmacology, Universita" degli Studi di Ferrara (Ferrara, Italy).
Member of the American Society of Human Genetics since 2004, Member of the America Association for Cancer Research since 2006
Member of the teaching staff of TIGEM doctorate program in Human Genetics, Open University UK, Medical Genetics at I University of Medicine (SUN) of Naples.
2003: Member of the American Society for Cell Biology
2004: Temporary Teacher at Federico II University of Medicine, Professor in Medical Genetics.
2005 "2006: Researcher, in a training program for Group Leader (MIUR) at CEINGE, Naples, Italy
November 2006-present: Associate Professor in Genetics and Medical Genetics (Bio/18), Faculty of Biotechnological Sciences, Federico II, Naples, Italy
1. Cimmino F, Schulte JH, Zollo M, Koster J, Versteeg R, Iolascon A, Eggert A, Schramm A.Galectin-1 is a major effector of TrkB-mediated neuroblastoma aggressiveness. Oncogene. 2009 May 14;28(19):2015-23. Epub 2009 Apr 13. ISSN: 0950-9232
2. Galasso A, Zollo M. The Nm23-H1-h-Prune complex in cellular physiology: a 'tip of the iceberg' protein network perspective.Mol Cell Biochem. Sep;329(1-2):149-59. ISSN: 1573-4919. 2009.
3. Müller T, Stein U, Poletti A, Garzia L, Rothley M, Plaumann D, Thiele W, Bauer M, Galasso A, Schlag P, Pankratz M, Zollo M, Sleeman JP ASAP1 promotes tumor cell motility and invasiveness, stimulates metastasis formation in vivo, and correlates with poor survival in colorectal cancer patients. Oncogene. 2010 Apr 22;29(16):2393-403. Epub 2010 Feb 15.
4. Andolfo I, De Falco L, Asci R, Russo R, Colucci S, Gorrese M, Zollo M, Iolascon A. Regulation of Divalent Metal Transporter 1 (DMT1) non-IRE isoform by the microRNA Let-7d in erythroid cells. Haematologica. 2010 Apr 21.
5. Castelletti D, Fiaschetti G, Di Dato V, Ziegler U, Kumps C, De Preter K, Zollo M, Speleman F, Shalaby T, De Martino D, Berg T, Eggert A, Arcaro A, Grotzer MA. The quassinoid derivative NBT-272 targets both the AKT and ERK signaling pathways in embryonal tumors. Mol Cancer Ther. 2010 Oct 1.
6. D Frezzetti, MD Menna, P Zoppoli, C Guerra, A Ferraro, AM Bello, P De Luca, C Calabrese, A Fusco,M Ceccarelli,M Zollo,M Barbacid, R Di Lauro and G De Vita. Upregulation of miR-21 by Ras in vivo and its role in tumor growth Oncogene. 2011 Jan 20;30(3):275-86.
7. Mestdagh P, Boström AK, Impens F, Fredlund E, Van Peer G, De Antonellis P, von Stedingk K, Ghesquière B, Schulte S, Dews M, Thomas-Tikhonenko A, Schulte JH, Zollo M, Schramm A, Gevaert K, Axelson H, Speleman F, Vandesompele J. The miR-17-92 microRNA cluster regulates multiple components of the TGF-β pathway in neuroblastoma. Mol Cell. 2010 Dec 10;40(5):762-73.
8. M. Zollo, I. Andolfo, P. DeAntonellis. Cancer Stem Cells Theories and Practice (ISBN 978-953-307-225-8) Review: MicroRNAs and Cancer Stem Cells in Medulloblastoma (2011)
9. Andolfo I, Petrosino G, Vecchione L, De Antonellis P, Capasso M, Montanaro D, Gemei M, Troncone G, Iolascon A, Orditura M, Ciardiello F, De Vita F, Zollo M. Detection of erbB2 copy number variations in plasma of patients with esophageal carcinoma BMC Cancer. 2011 Apr 11;11(1):126.
10. Andolfo I, De Martino D, Liguori L, Petrosino G, Troncone G, Tata N, Galasso A, Roma C, Chiancone F, Zarrilli S, Arrigoni G, Staibano S, Imbimbo C, Zollo M. Correlation of NM23-H1 cytoplasmic expression with metastatic stage in human prostate cancer tissue. Naunyn Schmiedebergs Arch Pharmacol. 2011 May 7.
11. Steeg PS, Zollo M, Wieland T. A critical evaluation of biochemical activities reported for the nucleoside diphosphate kinase/Nm23/Awd family proteins: opportunities and missteps in understanding their biological functions. Naunyn Schmiedebergs Arch Pharmacol. 2011 May 25.
Project Title:
miR34a functional regulation within the control of neuroblastoma tumor growth : a proteome analysis.
A class of non-­‐coding-­‐protein small RNAs, namely microRNAs (miRNAs), provide new insights in cancer research and therapeutics following a one hit-­‐multiple target pharmacological approach. MiRNAs negatively regulate the stability and translation of target mRNA molecules through binding their 3’UTR and have been implicated in a variety of processes such as cellular differentiation, cell cycle control , apoptosis and cancer . In mammals, the miR-­‐34 family comprises three processed miRNAs that are encoded by two different genes: miR-­‐34a is encoded by its own transcript, whereas miR-­‐34b and miR-­‐34c share a common primary transcript. In mice, miR-­‐34a is ubiquitously expressed, with the highest expression in brain. Earlier analyses also showed that miR-­‐34a is expressed at higher levels than miR-­‐34b/c, with the exception of the lung, in which miR-­‐34b/c is dominantly expressed. The importance of miR-­‐34a in cancer is now firmly established, having tumor suppressive effects in multiple types of cancer, including leukemias, hepatocellular carcinoma, pancreatic and colon, among others. Notably, miR-­‐34a is directly up-­‐regulated by p53 and a related family member, and miR-­‐34b and miR-­‐34c also have tumor suppressive effects. MiR-­‐ 34a maps to the distal region of chromosome 1p which is commonly deleted in neuroblastoma and was first identified as having a tumor suppressive function in this cancer. Tumors with loss of 1p are more commonly of the MYCN amplified variety. Ectopic over-­‐expression of miR-­‐34a in neuroblastoma cell lines resulted in the activation of a caspase-­‐mediated apoptotic pathway. Therefore, miR-­‐34a may be an important mediator of p53’s tumor-­‐suppressive activities. However, it is likely that miR-­‐34a regulates additional, as yet unconfirmed targets, since bioinformatic predictions suggest that several hundreds of mRNAs contain matches to the miR-­‐34a seed sequence. Our research group is deeply involved in the identification of miRNAs and their targets that are involved in regulation and control of embryonal tumors.
Because miR34a controls several proteins within cell cycle (c-­‐MYC, E2F, CDK4, CDK6, c-­‐MET), apoptosis (Bcl2, SIRT1) and cell differentiation impairing stem cell status (Notch1, Jag1, Dll1), we here intend to investigate the proteomic variation upon miR34a expression, which will give us insight into the activation and inhibition of pathways of relevance for cancer therapeutics.
We have generated several miR-­‐34a tetracycline inducible clones in both SH-­‐ SY5Y and SHEP NB cell lines. Those clones are important for defining the pathways that are up-­‐ or down regulated upon miR-­‐34a expression, and further of great importance. Proteomics can detect and quantify changes in protein expression induced by miRNA activation. We have investigated the effects of miR-­‐34a activation on the proteome of NB cancer cells using SILAC labelling followed by quantitative shotgun proteomics. The results obtained already will be given a global picture by system-­‐biology and computational approaches on miR34a regulating the network of several downstream pathways that can be used as a model to describe how miRNAs might control tumorigenesis during cancer progression.