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[Cancer Research 61, 7204-7210, October 1, 2001]
© 2001 American Association for Cancer Research

Experimental Therapeutics

Expression of CD26 and Its Associated Dipeptidyl Peptidase IV Enzyme Activity Enhances Sensitivity to Doxorubicin-induced Cell Cycle Arrest at the G2/M Checkpoint1

Ugur Aytac, Francois-Xavier Claret, Linus Ho, Kazuya Sato, Kei Ohnuma, Gordon B. Mills, Fernando Cabanillas, Chikao Morimoto and Nam H. Dang2

Departments of Lymphoma/Myeloma [U. A., K. S., F. C., N. H. D.], Gastrointestinal Oncology [L. H.], and Molecular Therapeutics [F-X. C., G. B. M., N. H. D.], M. D. Anderson Cancer Center, Houston, Texas 77030; and Department of Clinical Immunology and AIDS Research Center, Institute of Medical Science-University of Tokyo 4-6-1, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan [K. O., C. M.]

CD26, a Mr 110,000 surface-bound ectopeptidase with dipeptidyl peptidase IV (DPPIV) activity, has an array of diverse functional properties, with a role in T-cell physiology and the development of certain human cancers. In this study, we report that surface expression of CD26, through its associated DPPIV enzyme activity, enhanced sensitivity of Jurkat T-cell transfectants to G2-M arrest induced by the chemotherapeutic drug, doxorubicin. This was associated with disruption of cell cycle-related events, including hyperphosphorylation and inhibition of p34cdc2 kinase activity, phosphorylation of cdc25C, and alteration in cyclin B1 expression. In addition, we demonstrate that the addition of exogenous soluble DPPIV enhanced sensitivity of lymphoid tumor cell lines to doxorubicin, suggesting a potentially useful clinical role for CD26/DPPIV in the treatment of selected human hematological malignancies.




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