Open AccessEffect of CD38 on the multidrug resistance of human chronic myelogenous leukemia K562 cells to doxorubicin
Author(s) -
Leman Yalçıntepe,
Emre Halis,
Sibel Ulku
Publication year - 2016
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2016.4165
Subject(s) - k562 cells , multiple drug resistance , chronic myelogenous leukemia , doxorubicin , cd38 , pharmacology , leukemia , p glycoprotein , cancer cell , biology , cancer research , drug resistance , cancer , chemistry , immunology , microbiology and biotechnology , chemotherapy , stem cell , genetics , cd34
Drug resistance is a serious challenge in cancer chemotherapy. Alterations in the intracellular concentration and homeostasis of calcium (Ca 2+ ) may contribute to the development of drug resistance. To investigate the mechanism of drug resistance in leukemia, the present study rendered human chronic myelogenous leukemia K562 cells resistant to the cytotoxic effect of doxorubicin by progressively adapting the sensitive parental K562 cells to doxorubicin. The resulting cells were termed K562/DOX. Subsequently, the expression of two multidrug resistance proteins, P-glycoprotein (P-gp) and multidrug resistance protein 1 (MRP1), was analyzed in K562/DOX cells. In addition to P-gp and MRP1, these cells also expressed cluster of differentiation (CD)38 and its active enzyme adenosine diphosphate (ADP)-ribosyl cyclase. The present study also demonstrated that K562/DOX cells responded to cyclic ADP-ribose-mediated increases in intracellular Ca 2+ . These data indicate that CD38 may participate in the development of drug resistance to doxorubicin in K562 cells.