These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Establishment of a daunorubicin-resistant cell line which shows multi-drug resistance by multifactorial mechanisms.
    Author: Urasaki Y, Ueda T, Yoshida A, Fukushima T, Takeuchi N, Tsuruo T, Nakamura T.
    Journal: Anticancer Res; 1996; 16(2):709-14. PubMed ID: 8687117.
    Abstract:
    We established a daunorubicin (DNR)-resistant cell line derived from human leukemia cell line K562, (K562/D1-9), which also shows multidrug resistance (MDR). K562 cells were cultured with serially increasing concentrations up to 1.0 microM of DNR and then cloned by the limiting dilution method. K562/D1-9 cells were found to be 28 times more resistant to DNR than their its parent cells. Intracellular accumulation of DNR in K562/D1-9 was less than in the wild type, and P-glycoprotein (PGP) was overexpressed. Both DNR resistance and its intracellular accumulation were partially reversed by addition of verapamil to K562/D1-9 cells, but not to K562 cells. Topoisomerase II (Topo II) activity was decreased in K562/D1-9 cells. In contrast to other drugs, such as doxorubicin and vincristine, verapamil could not reverse drug resistance to VP-16 in the K562/D1-9 cell line, suggesting the importance of Topo II as the target of MDR. Protein kinase C (PKC) level was higher in K562/D1-9 than in K562. These findings suggested that the mechanism of MDR in this cell line might be multifactorial, including PGP, topo II and PKC. The K562/D1-9 cell line may be a good model for studying drug resistance in leukemia chemotherapy.
    [Abstract] [Full Text] [Related] [New Search]