Regulation of volume-sensitive Cl− channels in multi-drug resistant MCF7 cells

Marin, Matthieu; Poret, Agnès; Maillet, Géraldine; Leboulenger, F.; Foll, Frank Le

doi:10.1016/j.bbrc.2005.07.010

Cited by 13 publications

(12 citation statements)

References 44 publications

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“…Cultured cells were incubated at 37°C under a water-saturated 95% air, 5% CO 2 atmosphere. Exposure of MCF-7/DOXO to the P-gp inhibitors verapamil or cyclosporine A dose-dependently abolished both resistance to doxorubicin and P-gp activity in MCF-7/doxo (27).…”

Section: Methodsmentioning

confidence: 95%

Different Modalities of Intercellular Membrane Exchanges Mediate Cell-to-cell P-glycoprotein Transfers in MCF-7 Breast Cancer Cells

Pasquier¹,

Galas²,

Boulangé-Lecomte³

et al. 2012

Journal of Biological Chemistry

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124

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Background:The P-glycoprotein is expressed in many human cancers, where it contributes to multi-drug resistance phenomenon. Results: Both TnTs and microparticles contribute to the transfer of P-gp in MCF-7. Conclusion: Our findings supply new mechanistic evidences for the extragenetic emergence of MDR in cancer cells. Significance: Inhibition of both MPs and TnTs could be included in treatment strategies designed to overcome MDR.

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Section: Methodsmentioning

confidence: 95%

Different Modalities of Intercellular Membrane Exchanges Mediate Cell-to-cell P-glycoprotein Transfers in MCF-7 Breast Cancer Cells

Pasquier¹,

Galas²,

Boulangé-Lecomte³

et al. 2012

Journal of Biological Chemistry

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124

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“…In both a rat colon cancer cell line and its multidrug-resistant counterpart, cell-swelling activated Cl À currents could be detected (De Greef et al, 1995). VSOR Cl À current was observed in both multidrug-resistant and non-resistant variants of the human breast cancer MCF7 cell line (Marin et al, 2005). What changes are responsible for the loss of VSOR Cl À channel activity in the cisplatin-resistant cells?…”

Section: Journal Of Cellular Physiology Doi 101002/jcp C L à C H a Nmentioning

confidence: 96%

Impaired activity of volume‐sensitive Cl⁻ channel is involved in cisplatin resistance of cancer cells

Lee

Shimizu

Ise

et al. 2006

Journal Cellular Physiology

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The platinum-based drug cisplatin is a widely used anticancer drug which acts by causing the induction of apoptosis. However, resistance to the drug is a major problem. In this study we show that the KCP-4 human epidermoid cancer cell line, which serves as a model of acquired resistance to cisplatin, has virtually no volume-sensitive, outwardly rectifying (VSOR) chloride channel activity. The VSOR chloride channel's molecular identity has not yet been determined, and semi-quantitative RT-PCR experiments in this study suggested that the channel corresponds to none of three candidate genes. However, because it is known that the channel current plays an essential role in apoptosis, we hypothesized that lack of the current contributes to cisplatin resistance in these cells and that its restoration would reduce resistance. To test this hypothesis, we attempted to restore VSOR chloride current in KCP-4 cells. It was found that treatment with trichostatin A (TSA), a histone deacetylase inhibitor, caused VSOR chloride channel function to be partially restored. Treatment of the cells with both TSA and cisplatin resulted in an increase in caspase-3 activity at 24 h and a decrease in cell viability at 48 h. These effects were blocked by simultaneous treatment of the cells with a VSOR chloride channel blocker. These results indicate that restoration of the channel's functional expression by TSA treatment leads to a decrease in the cisplatin resistance of KCP-4 cells. We thus conclude that impaired activity of the VSOR chloride channel is involved in the cisplatin resistance of KCP-4 cancer cells.

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“…8B). For each tested cell, the activation kinetic could be fitted by a Boltzmann function as previously described (36). Surprisingly, the time for half-maximum activation (T o ) was dramatically augmented in HEK-SIG cells.…”

Section: Sigma-1 Receptor Expression Alters Vrcc Activation Propertiementioning

confidence: 99%

Cancer Cell Cycle Modulated by a Functional Coupling between Sigma-1 Receptors and Cl– Channels

Renaudo¹,

L’Hoste²,

Guizouarn

et al. 2007

Journal of Biological Chemistry

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The sigma-1 receptor is an intracellular protein characterized as a tumor biomarker whose function remains mysterious. We demonstrate herein for the first time that highly selective sigma ligands inhibit volume-regulated chloride channels (VRCC) in small cell lung cancer and T-leukemia cells. Sigma ligands and VRCC blockers provoked a cell cycle arrest underlined by p27 accumulation. In stably sigma-1 receptor-transfected HEK cells, the proliferation rate was significantly lowered by sigma ligands when compared with control cells. Sigma ligands produced a strong inhibition of VRCC in HEK-transfected cells but not in control HEK. Surprisingly, the activation rate of VRCC was dramatically delayed in HEK-transfected cells in the absence of ligands, indicating that sigma-1 receptors per se modulate cell regulating volume processes in physiological conditions. Volume measurements in hypotonic conditions revealed indeed that the regulatory volume decrease was delayed in HEK-transfected cells and virtually abolished in the presence of igmesine in both HEK-tranfected and T-leukemic cells. Moreover, HEKtransfected cells showed a significant resistance to staurosporine-induced apoptosis volume decrease, indicating that sigma-1 receptors protect cancer cells from apoptosis. Altogether, our results show for the first time that sigma-1 receptors modulate "cell destiny" through VRCC and cell volume regulation.Sigma receptors are intracellular proteins that were first postulated as opioid receptors on the basis of pharmacological and behavioral studies (1). Finally, 20 years of pharmacological studies and the cloning of the sigma-1 receptor subtype in 1996 revealed indeed that the "sigma-binding site" corresponded to a 24-kDa protein unrelated to other mammalian proteins and localized in the inner face of the plasma membrane and the membranes of the endoplasmic reticulum and the nucleus (2-5). Although high concentrations of neurosteroids have been shown to interact with brain sigma-1 receptors in behavioral studies (for review see Ref. 6), no high affinity endogene sigma ligand has been identified yet. Nonetheless, exogene compounds from disparate chemical classes ((ϩ)-benzomorphans, cocaine, guanidines, and neuroleptics for example) have been characterized or developed as highly selective sigma ligands (7). The sigma-1 receptors are expressed in various tissues including the brain, the pituitary, and the liver (2, 8 -10). Surprisingly, very high levels of sigma receptors have been detected in tumor cells when compared with normal cells (11,12). Indeed, the expression of sigma receptors in cancer biopsies is correlated with the proliferating state of the cells so that these proteins are now commonly considered to be tumor biomarkers (13,14). Consequently, many sigma ligands are developed nowadays for imagery (positon emission tomography scan) to detect early stage tumors (15, 16). However, if sigma receptors represent exciting targets to detect cancers in vivo, very few data are available on both the function and the action m...

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Regulation of volume-sensitive Cl− channels in multi-drug resistant MCF7 cells

Cited by 13 publications

References 44 publications

Different Modalities of Intercellular Membrane Exchanges Mediate Cell-to-cell P-glycoprotein Transfers in MCF-7 Breast Cancer Cells

Different Modalities of Intercellular Membrane Exchanges Mediate Cell-to-cell P-glycoprotein Transfers in MCF-7 Breast Cancer Cells

Impaired activity of volume‐sensitive Cl⁻ channel is involved in cisplatin resistance of cancer cells

Cancer Cell Cycle Modulated by a Functional Coupling between Sigma-1 Receptors and Cl– Channels

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Regulation of volume-sensitive Cl− channels in multi-drug resistant MCF7 cells

Cited by 13 publications

References 44 publications

Different Modalities of Intercellular Membrane Exchanges Mediate Cell-to-cell P-glycoprotein Transfers in MCF-7 Breast Cancer Cells

Different Modalities of Intercellular Membrane Exchanges Mediate Cell-to-cell P-glycoprotein Transfers in MCF-7 Breast Cancer Cells

Impaired activity of volume‐sensitive Cl− channel is involved in cisplatin resistance of cancer cells

Cancer Cell Cycle Modulated by a Functional Coupling between Sigma-1 Receptors and Cl– Channels

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Impaired activity of volume‐sensitive Cl⁻ channel is involved in cisplatin resistance of cancer cells