Abstract：
:Multidrug-resistant Chinese hamster ovary cell clones stably transfected with, and overexpressing, the mouse mdr1 complementary DNA clone along with drug-sensitive Chinese hamster ovary control cells were characterized for their capacities to accumulate and retain [3H]vinblastine. Multidrug-resistant mdr1 transfectants show a 3-4-fold decrease in [3H]vinblastine accumulation, compared to their drug-sensitive counterparts. After ATP depletion, this difference in [3H]vinblastine accumulation between mdr1 transfectants and control cells effectively disappears. This ATP-dependent decreased drug accumulation is paralleled in mdr1 transfectants by an enhanced capacity of these cells to extrude the drug in an ATP-dependent manner. In medium containing glucose and glutamine, the mdr1 transfectants release preloaded drug at a rate five times that of control, drug-sensitive cells. In ATP-depleted control and mdr1-transfected cells, there is little difference in the rate or extent of [3H]vinblastine release. The observation that the mdr1 transfectants show a decreased [3H]vinblastine accumulation and an increased vinblastine release, both of which are abolished when cellular ATP levels are reduced, provides a direct demonstration that the product of the transfected mdr1 gene is responsible for a mechanism controlling cellular drug levels in an ATP-dependent manner. However, attempts to establish competition for [3H]vinblastine transport by vincristine, daunomycin, and actinomycin D were only partly successful in mdr1 transfectants.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Hammond JR,Johnstone RM,Gros Psubject
Has Abstractpub_date
1989-07-15 00:00:00pages
3867-71issue
14eissn
0008-5472issn
1538-7445journal_volume
49pub_type
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