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Am J Physiol Lung Cell Mol Physiol 276: L679-L687, 1999;
1040-0605/99 $5.00
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Vol. 276, Issue 4, L679-L687, April 1999

Abrogation of cyclin D1 expression predisposes lung cancer cells to serum deprivation-induced apoptosis

Barbara Driscoll1, Susan Buckley1, Lora Barsky2, Kenneth Weinberg2, Kathryn D. Anderson1, and David Warburton1

1 Department of Surgery and Cell and Developmental Biology Program and 2 Department of Immunology/Bone Marrow Transplant, Childrens Hospital Los Angeles Research Institute, University of Southern California School of Medicine, Los Angeles, California 90027

Cyclin D1 antisense (D1AS)-transfected lung epithelial cell lines were serum deprived and then analyzed for three hallmarks of apoptosis: appearance of single-strand DNA breaks, alteration of apoptosis-related protein expression, and induction of chromatin condensation. Single-strand DNA breaks appeared at significant levels 24 h after serum deprivation, whereas induction of chromatin condensation was observed after 72 h. The antioxidants dimethyl sulfoxide, ascorbate, and glutathione, as well as insulin-like growth factor-I, inhibited induction of DNA damage in this assay. Additionally, proliferating cell nuclear antigen expression is completely suppressed in the D1AS cells, indicating a mechanism to explain the reduced capacity for DNA repair. Increased expression of cyclin D1, which is a common lesion in lung cancer, may thus prevent induction of apoptosis in an oxidizing and growth factor-poor environment. Reducing cyclin D1 expression in lung cancer cells by expression of D1AS RNA disrupted these protective pathways.

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