Role of the vacuolar H+-ATPase in daunorubicin distribution in etoposide-resistant MCF7 cells overexpressing the multidrug-resistance associated protein.

Benderra, Zineb; Morjani, Hamid; Trussardi, Aurélie; Manfait, Michel

doi:10.3892/ijo.12.3.711

Cited by 13 publications

(11 citation statements)

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“…72 Other modulators such as genistein, a specific inhibitor of tyrosine kinase, or 7-chloro-4-notrobenz-2-oxa-1,3-diazole (NBD), a vacuolar H+-ATPase, have been reported to modulate MRP1 of a non-specific manner. [73][74][75] However, genistein showed major differences in effects on Rh123 vs DNR transport in the MRP1-mediated MDR cell lines: the accumulation of DNR was increased, whereas the accumulation of Rh123 was decreased by genistein. 73 Recently, van der Kolk et al 40 and ourselves 11 have demonstrated that MRP1 was functional in fresh acute myeloid leukemic blast cells using CF and calcein-AM, respectively.…”

Section: Mrp1 Activity In Amlmentioning

confidence: 97%

Role of MRP1 in multidrug resistance in acute myeloid leukemia

1999

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The best characterized resistance mechanism in adult acute myeloid leukemia (AML) is the one mediated by the MDR1 gene which has been shown to be associated with poor outcome. However, alternative proteins such as the more recently recognized multidrug-associated protein (MRP1), may also contribute to the resistance to anthracyclines and etoposide in AML. Recently, the role of this protein was discussed and was unclear in AML. However, recent data concerning the functionality and the modulation of the activity of MRP1 may elucidate its role in comparison with other mechanisms of resistance. In this paper, we will review these recent data concerning the role of MRP1 in adult AML.

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Section: Mrp1 Activity In Amlmentioning

confidence: 97%

Role of MRP1 in multidrug resistance in acute myeloid leukemia

1999

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“…It also has to be emphasized that overexpression of Pgp is not the only reason for the appearance of the MDR phenotype. The MDR cells frequently express other efflux proteins, such as MRP (Zaman et al, 1995;Hayes and Pulford 1995), have high levels of H + -ATPase (Benderra et al, 1998) and exhibit the activated glutathione/ glutathione S-transferase detoxification system (Altan et al, 1998). These and possibly other factors could impose high energy requirements in MDR cells and collectively contribute to the elevated responsiveness of these cells to Pluronic.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of sensitization of MDR cancer cells by Pluronic block copolymers: Selective energy depletion

et al. 2001

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This paper, for the first time, demonstrates that exposure of cells to the poly(ethylene oxide)-poly(propylene oxide) block copolymer, Pluronic P85, results in a substantial decrease in ATP levels selectively in MDR cells. Cells expressing high levels of functional P-glycoprotein (MCF-7/ADR, KBv; LLC-MDR1; Caco-2, bovine brain microvessel endothelial cells [BBMECs]) are highly responsive to Pluronic treatment, while cells with low levels of P-glycoprotein expression (MCF-7, KB, LLC-PK1, human umbilical vein endothelial cells [HUVECs] C2C12 myoblasts) are much less responsive to such treatment. Cytotoxicity studies suggest that Pluronic acts as a chemosensitizer and potentiates cytotoxic effects of doxorubicin in MDR cells. The ability of Pluronic to inhibit P-glycoprotein and sensitize MDR cells appears to be a result of ATP depletion. Because many mechanisms of drug resistance are energy dependent, a successful strategy for treating MDR cancer could be based on selective energy depletion in MDR cells. Therefore, the finding of the energy-depleting effects of Pluronic P85, in combination with its sensitization effects is of considerable theoretical and practical significance. © 2001 Cancer Research Campaign http://www.bjcancer.com

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“…4A and B). MCF7 cells are known to have a greater capacity to regulate their pHi and lower sensitivity to the cytostatic effects of cariporide and S3705 (20,27,28), and this may contribute to their resistance to these compounds. The present experiments were undertaken to provide an in vitro model to evaluate the therapeutic potential of new inhibitors of regulation of pHi on the net killing of tumor cells by melphalan.…”

Section: Discussionmentioning

confidence: 99%

Reduction of Intracellular pH as a Strategy to Enhance the pH-Dependent Cytotoxic Effects of Melphalan for Human Breast Cancer Cells

Wong

Lee

Tannock

2005

Clinical Cancer Research

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The microenvironment within solid tumors is slightly acidic, and manipulation of this extracellular acidity to cause intracellular acidification might be used to increase selective antitumor effects of some anticancer drugs. Potential mechanisms include inhibition of repair of DNA damage and inhibition of repopulation of tumor cells between successive courses of chemotherapy. Here, we evaluate the influence of extracellular pH (pHe) and of two agents that lead to intracellular acidification (cariporide and S3705) on toxicity of melphalan for two human breast cancer cell lines (MDA-MB231and MCF7). Both the total number and number of colony-forming cells were evaluated during and after three sequential weekly drug treatments. Our results indicate the following: (a) Slow or absent repopulation after the first course of treatment that is influenced minimally by pHe. (b) Rapid repopulation after the second course of treatment that may be inhibited at low pHe. (c) Effects of low pHe following treatment with melphalan to increase cell kill. (d) Small effects of incubation in cariporide and S3705 at low pHe to increase the net cell kill after treatment with melphalan. Although these results add to evidence that manipulation of intracellular pH within the acidic environment of solid tumors can influence the effects of chemotherapy, they are too small and inconsistent to warrant clinical evaluation.

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Role of the vacuolar H+-ATPase in daunorubicin distribution in etoposide-resistant MCF7 cells overexpressing the multidrug-resistance associated protein.

Cited by 13 publications

References 0 publications

Role of MRP1 in multidrug resistance in acute myeloid leukemia

Role of MRP1 in multidrug resistance in acute myeloid leukemia

Mechanism of sensitization of MDR cancer cells by Pluronic block copolymers: Selective energy depletion

Reduction of Intracellular pH as a Strategy to Enhance the pH-Dependent Cytotoxic Effects of Melphalan for Human Breast Cancer Cells

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