Fhit Nuclear Import Following EGF Stimulation Sustains Proliferation of Breast Cancer Cells

Author:

Bianchi Francesca12,Sasso Marianna1,Turdo Federica1,Beretta Giovanni L.3,Casalini Patrizia1,Ghirelli Cristina1,Sfondrini Lucia2,Ménard Sylvie1,Tagliabue Elda1,Campiglio Manuela1

Affiliation:

1. Molecular Targeting Unit; Department of Experimental Oncology and Molecular Medicine; Fondazione IRCCS Istituto Nazionale dei Tumori; Milan Italy

2. Dipartimento di Scienze Biomediche per la Salute; Università degli Studi di Milano; Milan Italy

3. Molecular Pharmacology Unit; Department of Experimental Oncology and Molecular Medicine; Fondazione IRCCS Istituto Nazionale dei Tumori; Milan Italy

Funder

Associazione Italiana per la Ricerca sul Cancro (AIRC)

Publisher

Wiley

Subject

Cell Biology,Clinical Biochemistry,Physiology

Reference29 articles.

1. FHIT-proteasome degradation caused by mitogenic stimulation of the EGF receptor family in cancer cells;Bianchi;Proc Natl Acad Sci USA,2006

2. FHIT expression protects against HER2-driven breast tumor development: Unraveling the molecular interconnections;Bianchi;Cell Cycle,2007

3. FHIT loss of function in human primary breast cancer correlates with an advanced stage of the disease;Campiglio;Cancer Res,1999

4. Role of p53 in HER2-induced proliferation or apoptosis;Casalini;J Biol Chem,2001

5. Common fragile site tumor suppressor genes and corresponding mouse models of cancer;Drusco;J Biomed Biotechnol,2011

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