Cancer Research AACR Conference on Molecular Diagnostics - 2008 Tumor Immunology: New Perspectives
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[Cancer Research 61, 1578-1584, February 15, 2001]
© 2001 American Association for Cancer Research

Molecular Biology and Genetics

Effect of Adenoviral Transduction of the Fragile Histidine Triad Gene into Esophageal Cancer Cells1

Hideshi Ishii2, Kristoffel R. Dumon2, Andrea Vecchione2, Francesco Trapasso, Koshi Mimori, Hansjuerg Alder, Masaki Mori, Gabriella Sozzi, Raffaele Baffa, Kay Huebner and Carlo M. Croce3

Kimmel Cancer Institute, Jefferson Medical College of Thomas Jefferson University, Philadelphia, Pennsylvania 19107 [H. I., K. R. D., A. V., F. T., K. M., H. A., R. B., K. H., C. M. C.]; Medical Institute of Bioregulation, Kyushu University, Beppu, 874 Japan [K. M., M. M.]; and Istituto Nazionale Tumori, 20133, Milan, Italy [G. S.]

Reintroduction of a tumor suppressor gene product in cancer cells is a promising strategy for cancer gene therapy. The fragile histidine triad (FHIT) gene has been identified in a region at chromosome 3p14.2, which is deleted in many tumors, including esophageal cancer. Previous studies have shown frequent biallelic alterations of the FHIT gene in numerous tumors, and have demonstrated a tumor suppressor function of Fhit. We have studied the biological effects of adenoviral-FHIT transduction in esophageal cancer cell lines. Results showed suppression of cell growth in vitro in three of seven esophageal cancer cell lines, all seven of which showed abundant expression of the transgene. Adenoviral-FHIT expression, but not control adenoviral infections, induced caspase-dependent apoptosis in two esophageal cancer cell lines, TE14 and TE4, which express no or very little Fhit, respectively. Treatment of TE14 cells with adenoviral-FHIT vectors resulted in abrogation of tumorigenicity in nude mice. A third esophageal cancer cell line, TE12, without detectable endogenous Fhit, showed accumulation of cells at S to G2-M and a small apoptotic cell fraction after adenoviral-FHIT transduction. Thus, adenoviral-FHIT expression can inhibit the growth of esophageal cancer cells, at least in part through caspase-dependent apoptosis, suggesting that adenoviral-FHIT infection should be explored as a therapeutic strategy.




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Molecular Cancer Research Cancer Prevention Research
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Copyright © 2001 by the American Association for Cancer Research.