Differential involvement of glutathione S-transferase mu 1 and multidrug resistance protein 1 in melanoma acquired resistance to vinca alkaloids

Autor: Chaker Attaoua, Qiang Bai, Kamel Hadj-Kaddour, Aida Abdel Jaoued, John De Vos, Laure-Anaïs Vincent, Laurence Vian, Pierre Cuq
Přispěvatelé: Herrada, Anthony, Institut des Biomolécules Max Mousseron [Pôle Chimie Balard] (IBMM), Ecole Nationale Supérieure de Chimie de Montpellier (ENSCM)-Institut de Chimie du CNRS (INC)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Cellules Souches, Plasticité Cellulaire, Médecine Régénératrice et Immunothérapies (IRMB), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC)-Université de Montpellier (UM)-Ecole Nationale Supérieure de Chimie de Montpellier (ENSCM), Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier)
Jazyk: angličtina
Rok vydání: 2015
Předmět:
Vinca
Vindesine
Pharmacology
Biology
glutathione S-transferases
Vinblastine
vinca alkaloids
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Multidrug Resistance Protein 1
Gene expression
Tumor Cells
Cultured
medicine
melanoma
Humans
Pharmacology (medical)
neoplasms
Glutathione Transferase
030304 developmental biology
0303 health sciences
integumentary system
Melanoma
Vinorelbine
Glutathione
medicine.disease
biology.organism_classification
chemistry
Drug Resistance
Neoplasm
Glutathione S-Transferase Mu
Apoptosis
030220 oncology & carcinogenesis
[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology
Cancer research
[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology
Multidrug Resistance-Associated Proteins
multidrug resistance proteins
medicine.drug
Zdroj: Fundamental & Clinical Pharmacology
Fundamental & Clinical Pharmacology, 2015, 29 (1), pp.62-71. ⟨10.1111/fcp.12093⟩
Fundamental and Clinical Pharmacology
Fundamental and Clinical Pharmacology, Wiley, 2015, 29 (1), pp.62-71. ⟨10.1111/fcp.12093⟩
ISSN: 0767-3981
1472-8206
Popis: International audience; On account of its extreme intrinsic resistance to apoptosis and of its strong ability to become chemoresistant after a primary response to drugs, malignant melanoma (MM) is still a therapeutic challenge. We previously showed that glutathione S-transferase mu 1 (GSTM1) acts in synergy with multidrug resistance protein 1 (MRP1) to protect GSTM1-transfected human CAL1 melanoma cells from toxic effects of vincristine (VCR). Herein, we investigated the role of these proteins in the acquired resistance of CAL1 cells to vinca alkaloids (VAs). Resistant lines were established by continuous exposure (>1 year) of parental CAL1-wt cells to VCR, vindesine (VDS), or vinorelbine (VRB): CAL1R-VCR, CAL1R-VDS, CAL1R-VRB, respectively. All resistant lines displayed more than 10-fold increase in resistance to their selection VA, and specifically expressed GSTM1. Suggesting a direct interaction between this protein and VAs, each VA specifically decreased the GSTM1-mediated glutathione conjugation activity in cell lysates. Curcumin (GSTM1 inhibitor), BSO (glutathione synthesis inhibitor), and MK571 (MRP1 inhibitor) considerably reversed the acquired resistance to VCR and VDS, but not to VRB. Microarray data analysis revealed similar gene expression patterns of CAL1R-VCR and CAL1R-VDS, and a distinct one for CAL1R-VRB. These data suggest a differential involvement of GSTM1 and MRP1 in acquired resistance to VAs. A coordinated expression and activity of GSTM1 and MRP1 is required to protect CAL1 cells from VCR and VDS, while the simple expression of GSTM1 is sufficient, possibly by a direct drug/protein interaction, to confer resistance against VRB.
Databáze: OpenAIRE
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