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[Cancer Research 59, 3333-3339, July 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 3333-3339, July 15, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

Induction of Apoptosis and Inhibition of Tumorigenicity and Tumor Growth by Adenovirus Vector-mediated Fragile Histidine Triad (FHIT) Gene Overexpression1

Lin Ji, Bingliang Fang, Nancy Yen, Kwun Fong, John D. Minna and Jack A. Roth2

Section of Thoracic Molecular Oncology, Department of Thoracic and Cardiovascular Surgery, The University of Texas, M. D. Anderson Cancer Center, Houston, Texas 77030 [L. J., B. F., N. Y., J. A. R.], and Hamon Center for Therapeutic Oncology Research and Departments of Internal Medicine and Pharmacology, The University of Texas Southwestern Medical Center, Dallas, Texas 75235-8593 [K. F., J. D. M.]

We studied the effects of fragile histidine triad (FHIT) gene overexpression mediated by an adenoviral vector, Ad-FHIT, on cell proliferation, apoptosis, and cell cycle kinetics in human cancer cells and on tumorigenicity and tumor growth in nude mice. Overexpression of the FHIT gene significantly inhibited cell growth in various Ad-FHIT-transduced human lung cancer cells and head and neck carcinoma cells with FHIT gene abnormalities, but not in normal human bronchial epithelial cells. Fewer than 20% of cells in all Ad-FHIT-transduced cells survived at 7 days after transduction. Overexpression of the FHIT gene induced cell apoptosis and altered cell cycle processes. The apoptotic cell population markedly increased, and cells accumulated in S phase after Ad-FHIT transduction. The tumorigenicity of human H1299 lung cancer cells transduced by Ad-FHIT, in comparison with that of the control transductants and untreated cells, was eliminated in vivo. Subcutaneous tumor growth in nude mice who received intratumoral injections of Ad-FHIT, at a total dose of 3 x 1010 plaque-forming units/tumor for H1299 tumors and 4 x 1010/tumor for A549 tumors, were suppressed by more than 85% and 90%, respectively, compared with that in nude mice who received injections of empty vector at the same dose or with PBS alone. Together, our results suggest that the FHIT gene, when delivered at high efficiency by a recombinant adenoviral vector, functions as a tumor suppressor gene both in vitro and in vivo.




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