The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
P-Glycoprotein Protects Leukemia Cells Against Caspase-Dependent, but not Caspase-Independent, Cell Death
Abstract
A major problem with treating patients with cancer by traditional chemotherapeutic regimes is that their tumors often develop a multidrug resistant (MDR) phenotype and subsequently become insensitive to a range of different chemotoxic drugs. One cause of MDR is overexpression of the drug-effluxing protein, P-glycoprotein.It is now apparent that P-glycoprotein may also possess a more generic antiapoptotic function that protects P-glycoprotein–expressing cancer cells and normal cells from cell death. Herein we show that cells induced to express P-glycoprotein either by drug selection or by retroviral gene transduction with MDR1 cDNA are resistant to cell death induced by a wide range of death stimuli, such as FasL, tumor necrosis factor (TNF), and ultraviolet (UV) irradiation, that activate the caspase apoptotic cascade.However, P-glycoprotein–expressing cells were not resistant to caspase-independent cell death mediated by pore-forming proteins and granzyme B.MDR P-glycoprotein–expressing cells were made sensitive to caspase-dependent apoptosis by the addition of anti–P-glycoprotein antibodies or verapamil, a pharmacological inhibitor of P-glycoprotein function. Clonogenic assays showed that P-glycoprotein confers long-term resistance to caspase-dependent apoptotic stimuli but not to caspase-independent cell death stimuli. This study has confirmed a potential novel physiological function for P-glycoprotein and it now remains to dissect the molecular mechanisms involved in the inhibition of capsase-dependent cell death by P-glycoprotein.
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Metadata
- Authors
- Johnstone, R. W., Cretney, E., & Smyth, M. J.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 1999-02-01
- Volume
- 93
- Issue
- 3
- Pages
- 1075-1085
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W102593176
- Cited by
- 315
- References
- 44
- FWCI
- 9.40
- Type
- journal article
- Language
- en
- Open access
- closed
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