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Restoration of fragile histidine triad (FHIT) expression induces apoptosis and suppresses tumorigenicity in breast cancer cell lines.

Abstract
The fragile histidine triad (FHIT) gene at chromosome 3p14.2 is a tumor suppressor gene that is altered mainly by deletion in a large fraction of human tumors, including breast cancers. To evaluate the potential of FHIT gene therapy in this type of cancer, we have studied the biological effects of adenoviral FHIT transduction (Ad-FHIT) in breast cancer cell lines. The results showed that, after FHIT restoration in BT-549, MDA-MB-436, and HCC1806 cells, they underwent apoptosis by activation of the intrinsic pathway. In all three cell lines infected with Ad-FHIT, we have found activation of caspase-2, which is required for permeabilization of mitochondria, release of cytochrome c, and apoptosis. Furthermore, Fhit overexpression produces alteration in cell cycling properties, as well as reduction of the tumorigenic potential in nude mice.
AuthorsCinzia Sevignani, George A Calin, Rossano Cesari, Manuela Sarti, Hideshi Ishii, Sai Yendamuri, Andrea Vecchione, Francesco Trapasso, Carlo M Croce
JournalCancer research (Cancer Res) Vol. 63 Issue 6 Pg. 1183-7 (Mar 15 2003) ISSN: 0008-5472 [Print] United States
PMID12649173 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Neoplasm Proteins
  • fragile histidine triad protein
  • Acid Anhydride Hydrolases
Topics
  • Acid Anhydride Hydrolases
  • Adenoviridae (genetics)
  • Animals
  • Apoptosis (genetics)
  • Breast Neoplasms (genetics, metabolism, pathology, therapy)
  • Cell Cycle (genetics)
  • Cell Division (genetics)
  • Female
  • Genetic Therapy (methods)
  • Humans
  • Mice
  • Mice, Nude
  • Neoplasm Proteins (biosynthesis, genetics, physiology)
  • Transduction, Genetic
  • Tumor Cells, Cultured
  • Xenograft Model Antitumor Assays

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