Consequences of cell-to-cell P-glycoprotein transfer on acquired multidrug resistance in breast cancer: a cell population dynamics model
Identifieur interne : 000793 ( Main/Exploration ); précédent : 000792; suivant : 000794Consequences of cell-to-cell P-glycoprotein transfer on acquired multidrug resistance in breast cancer: a cell population dynamics model
Auteurs : Jennifer Pasquier ; Pierre Magal [France] ; Céline Boulangé-Lecomte ; Glenn Webb [États-Unis] ; Frank Le FollSource :
- Biology Direct [ 1745-6150 ] ; 2011.
English descriptors
- KwdEn :
- Algorithms, Breast Neoplasms (drug therapy), Breast Neoplasms (metabolism), Breast Neoplasms (pathology), Cell Communication (physiology), Cell Line, Tumor, Cell Proliferation (drug effects), Coculture Techniques, Computer Simulation, Doxorubicin (pharmacology), Drug Resistance, Multiple (physiology), Female, Flow Cytometry, Fluoresceins (metabolism), Fluorescent Dyes (metabolism), Humans, Kinetics, Models, Biological, P-Glycoprotein (metabolism), Protein Transport (physiology).
- MESH :
- chemical , metabolism : Fluoresceins, Fluorescent Dyes, P-Glycoprotein.
- chemical , pharmacology : Doxorubicin.
- drug effects : Cell Proliferation.
- drug therapy : Breast Neoplasms.
- metabolism : Breast Neoplasms.
- pathology : Breast Neoplasms.
- physiology : Cell Communication, Drug Resistance, Multiple, Protein Transport.
- Algorithms, Cell Line, Tumor, Coculture Techniques, Computer Simulation, Female, Flow Cytometry, Humans, Kinetics, Models, Biological.
Abstract
Cancer is a proliferation disease affecting a genetically unstable cell population, in which molecular alterations can be somatically inherited by genetic, epigenetic or extragenetic transmission processes, leading to a cooperation of neoplastic cells within tumoural tissue. The efflux protein P-glycoprotein (P-gp) is overexpressed in many cancer cells and has known capacity to confer multidrug resistance to cytotoxic therapies. Recently, cell-to-cell P-gp transfers have been shown. Herein, we combine experimental evidence and a mathematical model to examine the consequences of an intercellular P-gp trafficking in the extragenetic transfer of multidrug resistance from resistant to sensitive cell subpopulations.
We report cell-to-cell transfers of functional P-gp in co-cultures of a P-gp overexpressing human breast cancer MCF-7 cell variant, selected for its resistance towards doxorubicin, with the parental sensitive cell line. We found that P-gp as well as efflux activity distribution are progressively reorganized over time in co-cultures analyzed by flow cytometry. A mathematical model based on a Boltzmann type integro-partial differential equation structured by a continuum variable corresponding to P-gp activity describes the cell populations in co-culture. The mathematical model elucidates the population elements in the experimental data, specifically, the initial proportions, the proliferative growth rates, and the transfer rates of P-gp in the sensitive and resistant subpopulations.
We confirmed cell-to-cell transfer of functional P-gp. The transfer process depends on the gradient of P-gp expression in the donor-recipient cell interactions, as they evolve over time. Extragenetically acquired drug resistance is an additional aptitude of neoplastic cells which has implications in the diagnostic value of P-gp expression and in the design of chemotherapy regimens.
This article was reviewed by Leonid Hanin, Anna Marciniak-Czochra and Marek Kimmel.
Url:
DOI: 10.1186/1745-6150-6-5
PubMed: 21269489
PubMed Central: 3038988
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>Cancer is a proliferation disease affecting a genetically unstable cell population, in which molecular alterations can be somatically inherited by genetic, epigenetic or extragenetic transmission processes, leading to a cooperation of neoplastic cells within tumoural tissue. The efflux protein P-glycoprotein (P-gp) is overexpressed in many cancer cells and has known capacity to confer multidrug resistance to cytotoxic therapies. Recently, cell-to-cell P-gp transfers have been shown. Herein, we combine experimental evidence and a mathematical model to examine the consequences of an intercellular P-gp trafficking in the extragenetic transfer of multidrug resistance from resistant to sensitive cell subpopulations.</p>
</sec>
<sec><title>Methodology and Principal Findings</title>
<p>We report cell-to-cell transfers of functional P-gp in co-cultures of a P-gp overexpressing human breast cancer MCF-7 cell variant, selected for its resistance towards doxorubicin, with the parental sensitive cell line. We found that P-gp as well as efflux activity distribution are progressively reorganized over time in co-cultures analyzed by flow cytometry. A mathematical model based on a Boltzmann type integro-partial differential equation structured by a continuum variable corresponding to P-gp activity describes the cell populations in co-culture. The mathematical model elucidates the population elements in the experimental data, specifically, the initial proportions, the proliferative growth rates, and the transfer rates of P-gp in the sensitive and resistant subpopulations.</p>
</sec>
<sec><title>Conclusions</title>
<p>We confirmed cell-to-cell transfer of functional P-gp. The transfer process depends on the gradient of P-gp expression in the donor-recipient cell interactions, as they evolve over time. Extragenetically acquired drug resistance is an additional aptitude of neoplastic cells which has implications in the diagnostic value of P-gp expression and in the design of chemotherapy regimens.</p>
</sec>
<sec><title>Reviewers</title>
<p>This article was reviewed by Leonid Hanin, Anna Marciniak-Czochra and Marek Kimmel.</p>
</sec>
</div>
</front>
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<region><li>Aquitaine</li>
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