RapamycinFungusV1, Main, Exploration, bibRecord, 000C30

Rapid Identification of Chemoresistance Mechanisms Using Yeast DNA Mismatch Repair Mutants.

Identifieur interne : 000C30 ( Main/Exploration ); précédent : 000C29; suivant : 000C31

Rapid Identification of Chemoresistance Mechanisms Using Yeast DNA Mismatch Repair Mutants.

Auteurs : Irene Ojini [États-Unis] ; Alison Gammie [États-Unis]

Source :

G3 (Bethesda, Md.) [ 2160-1836 ] ; 2015.

RBID : pubmed:26199284

Descripteurs français

KwdFr :
- Benzopyranes (pharmacologie), Bibliothèques de petites molécules (MeSH), Chlorméthine (pharmacologie), Découverte de médicament (MeSH), Endocytose (effets des médicaments et des substances chimiques), Endocytose (génétique), Génome fongique (MeSH), Génomique (méthodes), Mutation (MeSH), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Réparation de mésappariement de l'ADN (MeSH), Résistance aux médicaments antinéoplasiques (MeSH), Saccharomyces cerevisiae (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Sphingolipides (biosynthèse), Séquençage nucléotidique à haut débit (MeSH), Tests de criblage d'agents antitumoraux (MeSH).
MESH :
- biosynthèse : Sphingolipides.
- effets des médicaments et des substances chimiques : Endocytose, Saccharomyces cerevisiae.
- génétique : Endocytose, Protéines de Saccharomyces cerevisiae, Saccharomyces cerevisiae.
- métabolisme : Protéines de Saccharomyces cerevisiae, Saccharomyces cerevisiae.
- méthodes : Génomique.
- pharmacologie : Benzopyranes, Chlorméthine.
- Bibliothèques de petites molécules, Découverte de médicament, Génome fongique, Mutation, Réparation de mésappariement de l'ADN, Résistance aux médicaments antinéoplasiques, Séquençage nucléotidique à haut débit, Tests de criblage d'agents antitumoraux.

English descriptors

KwdEn :
- Benzopyrans (pharmacology), DNA Mismatch Repair (MeSH), Drug Discovery (MeSH), Drug Resistance, Neoplasm (MeSH), Drug Screening Assays, Antitumor (MeSH), Endocytosis (drug effects), Endocytosis (genetics), Genome, Fungal (MeSH), Genomics (methods), High-Throughput Nucleotide Sequencing (MeSH), Mechlorethamine (pharmacology), Mutation (MeSH), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Small Molecule Libraries (MeSH), Sphingolipids (biosynthesis).
MESH :
- chemical , biosynthesis : Sphingolipids.
- chemical , genetics : Saccharomyces cerevisiae Proteins.
- chemical , metabolism : Saccharomyces cerevisiae Proteins.
- chemical , pharmacology : Benzopyrans, Mechlorethamine.
- drug effects : Endocytosis, Saccharomyces cerevisiae.
- genetics : Endocytosis, Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae.
- methods : Genomics.
- DNA Mismatch Repair, Drug Discovery, Drug Resistance, Neoplasm, Drug Screening Assays, Antitumor, Genome, Fungal, High-Throughput Nucleotide Sequencing, Mutation, Small Molecule Libraries.

Abstract

Resistance to cancer therapy is a major obstacle in the long-term treatment of cancer. A greater understanding of drug resistance mechanisms will ultimately lead to the development of effective therapeutic strategies to prevent resistance from occurring. Here, we exploit the mutator phenotype of mismatch repair defective yeast cells combined with whole genome sequencing to identify drug resistance mutations in key pathways involved in the development of chemoresistance. The utility of this approach was demonstrated via the identification of the known CAN1 and TOP1 resistance targets for two compounds, canavanine and camptothecin, respectively. We have also experimentally validated the plasma membrane transporter HNM1 as the primary drug resistance target of mechlorethamine. Furthermore, the sequencing of mitoxantrone-resistant strains identified inactivating mutations within IPT1, a gene encoding inositolphosphotransferase, an enzyme involved in sphingolipid biosynthesis. In the case of bactobolin, a promising anticancer drug, the endocytosis pathway was identified as the drug resistance target responsible for conferring resistance. Finally, we show that that rapamycin, an mTOR inhibitor previously shown to alter the fitness of the ipt1 mutant, can effectively prevent the formation of mitoxantrone resistance. The rapid and robust nature of these techniques, using Saccharomyces cerevisiae as a model organism, should accelerate the identification of drug resistance targets and guide the development of novel therapeutic combination strategies to prevent the development of chemoresistance in various cancers.

DOI: 10.1534/g3.115.020560
PubMed: 26199284
PubMed Central: PMC4555229

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<front><div type="abstract" xml:lang="en">Resistance to cancer therapy is a major obstacle in the long-term treatment of cancer. A greater understanding of drug resistance mechanisms will ultimately lead to the development of effective therapeutic strategies to prevent resistance from occurring. Here, we exploit the mutator phenotype of mismatch repair defective yeast cells combined with whole genome sequencing to identify drug resistance mutations in key pathways involved in the development of chemoresistance. The utility of this approach was demonstrated via the identification of the known CAN1 and TOP1 resistance targets for two compounds, canavanine and camptothecin, respectively. We have also experimentally validated the plasma membrane transporter HNM1 as the primary drug resistance target of mechlorethamine. Furthermore, the sequencing of mitoxantrone-resistant strains identified inactivating mutations within IPT1, a gene encoding inositolphosphotransferase, an enzyme involved in sphingolipid biosynthesis. In the case of bactobolin, a promising anticancer drug, the endocytosis pathway was identified as the drug resistance target responsible for conferring resistance. Finally, we show that that rapamycin, an mTOR inhibitor previously shown to alter the fitness of the ipt1 mutant, can effectively prevent the formation of mitoxantrone resistance. The rapid and robust nature of these techniques, using Saccharomyces cerevisiae as a model organism, should accelerate the identification of drug resistance targets and guide the development of novel therapeutic combination strategies to prevent the development of chemoresistance in various cancers. </div>
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Rapid Identification of Chemoresistance Mechanisms Using Yeast DNA Mismatch Repair Mutants.

Rapid Identification of Chemoresistance Mechanisms Using Yeast DNA Mismatch Repair Mutants.

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