Document Detail


Redox regulation of P-glycoprotein-mediated multidrug resistance in multicellular prostate tumor spheroids.
MedLine Citation:
PMID:  10629088     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Multicellular prostate tumor spheroids develop intrinsic P-glycoprotein (Pgp)-mediated multidrug resistance with the appearance of quiescent cell areas. We have investigated the effect of intracellular reactive oxygen species (ROS) on Pgp expression in large, quiescent and drug-resistant multicellular spheroids (diameter 250 +/- 50microm). Using the ROS-sensitive fluorescence dye 2;7;-dichlorodihydrofluorescein diacetate (H(2)DCFDA), we demonstrated that these tumor spheroids are characterized by reduced intracellular ROS compared with drug-sensitive small spheroids (diameter 60 +/- 20microm) consisting predominantly of proliferating cells. The prooxidants hydrogen peroxide, menadione and glyceraldehyde raised ROS in large tumor spheroids and significantly down-regulated Pgp within 24 hr. Comparable effects were achieved with the known Pgp-reversing agents sodium orthovanadate, quinidine and cyclosporin A but not with verapamil. Consequently, the retention and toxicity of the anthracycline doxorubicin was increased in tumor spheroids treated with prooxidants. Co-administration of prooxidants and the free radical scavenger ebselen did not alter Pgp levels, indicating that down-regulation of Pgp is mediated via ROS. Down-regulation of Pgp by H(2)O(2) was abolished when either forskolin, 8-Br-cAMP or IBMX, which raise intracellular cAMP levels, was co-administered, indicating that Pgp expression is regulated by protein kinase A (PKA). Furthermore, Pgp was down-regulated by the PKA inhibitors Rp-cAMPs and H89. Since prooxidants stimulated the growth of multicellular spheroids and down-regulated the cyclin-dependent kinase inhibitor p27(kip1), we conclude that ROS-mediated Pgp down-regulation may be paralleled by recruitment of drug-resistant quiescent cells in the depth of the tumor tissue for cell-cycle activity.
Authors:
M Wartenberg; K Fischer; J Hescheler; H Sauer
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of cancer. Journal international du cancer     Volume:  85     ISSN:  0020-7136     ISO Abbreviation:  Int. J. Cancer     Publication Date:  2000 Jan 
Date Detail:
Created Date:  2000-02-01     Completed Date:  2000-02-01     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0042124     Medline TA:  Int J Cancer     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  267-74     Citation Subset:  IM    
Copyright Information:
Copyright 2000 Wiley-Liss, Inc.
Affiliation:
Department of Neurophysiology, University of Cologne, Cologne, Germany.
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MeSH Terms
Descriptor/Qualifier:
Antineoplastic Agents / pharmacology
Cell Cycle / drug effects
Cell Cycle Proteins*
Cyclic AMP-Dependent Protein Kinases / metabolism
Cyclin-Dependent Kinase Inhibitor p27
Doxorubicin / pharmacology
Drug Resistance, Multiple*
Drug Resistance, Neoplasm*
Gene Expression Regulation, Neoplastic
Glyceraldehyde / pharmacology
Humans
Hydrogen Peroxide / pharmacology
Male
Microtubule-Associated Proteins / biosynthesis,  metabolism
Oxidants / pharmacology*
Oxidation-Reduction
P-Glycoprotein / genetics,  metabolism*
Phenotype
Prostatic Neoplasms / metabolism*,  pathology
Reactive Oxygen Species / metabolism*
Spheroids, Cellular / drug effects*,  metabolism,  pathology
Tumor Cells, Cultured
Tumor Suppressor Proteins*
Vitamin K / pharmacology
Chemical
Reg. No./Substance:
0/Antineoplastic Agents; 0/Cell Cycle Proteins; 0/Microtubule-Associated Proteins; 0/Oxidants; 0/P-Glycoprotein; 0/Reactive Oxygen Species; 0/Tumor Suppressor Proteins; 12001-79-5/Vitamin K; 147604-94-2/Cyclin-Dependent Kinase Inhibitor p27; 23214-92-8/Doxorubicin; 367-47-5/Glyceraldehyde; 7722-84-1/Hydrogen Peroxide; EC 2.7.11.11/Cyclic AMP-Dependent Protein Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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