Expression of CD26 and its associated dipeptidyl peptidase IV enzyme activity enhances sensitivity to doxorubicin-induced cell cycle arrest at the G2/M checkpoint

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

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    33 Scopus citations

    Abstract

    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.

    Original languageEnglish (US)
    Pages (from-to)7204-7210
    Number of pages7
    JournalCancer Research
    Volume61
    Issue number19
    StatePublished - Oct 1 2001

    ASJC Scopus subject areas

    • Oncology
    • Cancer Research

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    Aytac, U., Sato, K., Cabanillas, F., Dang, N. H., Ho, L., Claret, F. X., Mills, G. B., Dang, N. H., Ohnuma, K., & Morimoto, C. (2001). Expression of CD26 and its associated dipeptidyl peptidase IV enzyme activity enhances sensitivity to doxorubicin-induced cell cycle arrest at the G2/M checkpoint. Cancer Research, 61(19), 7204-7210.