Regulation of volume-sensitive Cl- channels in multi-drug resistant MCF7 cells.
Identifieur interne : 000C90 ( France/Analysis ); précédent : 000C89; suivant : 000C91Regulation of volume-sensitive Cl- channels in multi-drug resistant MCF7 cells.
Auteurs : Matthieu Marin [France] ; Agnès Poret ; Géraldine Maillet ; François Leboulenger ; Frank Le FollSource :
- Biochemical and biophysical research communications [ 0006-291X ] ; 2005.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Chloride Channels, P-Glycoprotein.
- metabolism : Breast Neoplasms.
- pathology : Breast Neoplasms.
- Cell Line, Tumor, Cell Size, Drug Resistance, Multiple, Humans, Ion Channel Gating, Water-Electrolyte Balance.
Abstract
The P-glycoprotein (P-gp) is thought to be involved in the regulation of volume-sensitive chloride channels. In this study, the possible coupling between P-gp and swelling-activated chloride channels has been examined in MCF7 cells with sensitive (MDR-), resistant (MDR+), and reversed resistant (MDR(REV)) phenotypes. Western blot analysis showed that incubation of cells with doxorubicin induced P-gp expression in a reversible manner. Exposure of MDR+ cells to hypotonicity resulted in an inhibition of P-gp activity while hypotonic challenges induced swelling-activated chloride currents (I(Cl-swell)) in MDR-, MDR+, and MDR(REV) MCF7 cells. While verapamil inhibited I(Cl-swell) in all cell types, doxorubicin and vincristine rapidly and reversibly inhibited I(Cl-swell) uniquely in MDR+. Intracellular dialysis of MDR+ cells with C219 anti-P-gp antibody abolished the sensitivity of I(Cl-swell) to doxorubicin and led to a response pattern very close to that of MDR- cells. Taken together, these results strongly suggest that the P-glycoprotein regulates I(Cl-swell) in resistant MCF7.
DOI: 10.1016/j.bbrc.2005.07.010
PubMed: 16039989
Affiliations:
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pubmed:16039989Le document en format XML
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<front><div type="abstract" xml:lang="en">The P-glycoprotein (P-gp) is thought to be involved in the regulation of volume-sensitive chloride channels. In this study, the possible coupling between P-gp and swelling-activated chloride channels has been examined in MCF7 cells with sensitive (MDR-), resistant (MDR+), and reversed resistant (MDR(REV)) phenotypes. Western blot analysis showed that incubation of cells with doxorubicin induced P-gp expression in a reversible manner. Exposure of MDR+ cells to hypotonicity resulted in an inhibition of P-gp activity while hypotonic challenges induced swelling-activated chloride currents (I(Cl-swell)) in MDR-, MDR+, and MDR(REV) MCF7 cells. While verapamil inhibited I(Cl-swell) in all cell types, doxorubicin and vincristine rapidly and reversibly inhibited I(Cl-swell) uniquely in MDR+. Intracellular dialysis of MDR+ cells with C219 anti-P-gp antibody abolished the sensitivity of I(Cl-swell) to doxorubicin and led to a response pattern very close to that of MDR- cells. Taken together, these results strongly suggest that the P-glycoprotein regulates I(Cl-swell) in resistant MCF7.</div>
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