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Review

Yeast as a model system for anticancer drug discovery

Pages 177-195 | Published online: 25 Feb 2005

Bibliography

  • ROWINSKY EK: The pursuit of optimal outcomes in cancer therapy in a new age of rationally designed target-based anticancer agents. Drugs (2000) 60:1–14.
  • SAUSVILLE EA, JOHNSON JI: Molecules for the millenium: how will they look? new drug discovery year 2000. Br.)'. Cancer (2000) 83:1401–1404.
  • ALLEY MC, SCUDIERO DA, MONKS A et al: Feasibility of drug screening with panels of human tumor cell lines using a microculture tetrazolium assay. Cancer Res. (1988) 48:589–601.
  • PAULL KD, SHOEMAKER RH, HODES L et al.: Display and analysis of patterns of differential activity of drugs against human tumor cell lines: development of mean graph and COMPARE algorithm. J. Natl. Cancer Inst. (1989) 81:1088–1092.
  • PANEK RL, LU GH, KLUTCHKO SR et al: In vitro pharma-cological characterization of PD 166285, a new nanomolar potent and broadly active protein tyrosine kinase inhibitor. J. Pharmacol. Exp. Ther. (1997) 283:1433–1444.
  • BRENNER C: A cultivated taste for yeast. Genome (2000) 1(0:103.
  • CARDENAS ME, CRUZ MC, DEL POETA M, CHUNG N, PERFECT JR, HEITMAN J: An tifungal activities of antineoplastic agents: Saccharomyces cerevisiae as a model system to study drug action. Clin. Microbiol. Rev. (1999) 12:583–611.
  • •An excellent review of mechanistic studies in yeast of several natural product anticancer antibiotics.
  • BASSETT DE, Jr., BOGUSKI MS, HIETER P: Yeast genes and human disease. Nature (1996) 379:589–590.
  • •An analysis of sequence similarities between cloned human disease genes and yeast genes.
  • RENAN MJ: How many mutations are required for tumorigenesis? Implications from human cancer data. Mol. Carcinog. (1993) 7:139–146.
  • HARTWELL LH, SZANKASI P, ROBERTS CJ, MURRAY AW, FRIEND SH: Integrating genetic approaches into the discovery of anticancer drugs. Science (1997) 278:1064–1068.
  • ••An excellent overview of the utility of yeast as a modelsystem for anticancer drug and drug target discovery using pharmacological, genetic and genomic strategies.
  • WHITE RJ: Microbiological models as screening tools for anticancer agents: potentials and limitations. Ann. Rev. Microbiol. (1982) 36:415–433.
  • ••An excellent historical overview of the use on microbio-logical models including virus, bacteria and yeast-based screens in the pharmaceutical industry.
  • WAKSMAN SA, TISHLER M: The chemical nature of actinomycin, an antimicrobial substance produced by Actin omyces antibioticus. J. Biol. Chem. (1942) 142:519–528.
  • ROSENBERG B, VANCAMP L, KRIGAS T: Inhibition of cell division in Escherichia colt by electrolysis products from a platinum electrode. Nature (1965) 205:698–699.
  • SIMON JA, SZANKASI P, NGUYEN DK et al.: Differential toxicities of anticancer agents among DNA repair and checkpoint mutants of Saccharomyces cerevisiae. Cancer Res. (2000) 60:328–333.
  • •A survey of 23 FDA-approved anticancer agents and x-rays tested against a panel of 21 yeast strains with defects in DNA repair and cell cycle control.
  • GOFFEAU A, BARRELL BG, BUSSEY H et al: life with 6000 genes. Science (1996) 274:546.
  • •Sequencing of the Saccharomyces cerevisiae genome.
  • TUGENDREICH S, BASSETT DE, JR., MCKUSICK VA, BOGUSKI MS, HIETER P: Genes conserved in yeast and humans. Hum. Mol. Genetics (1994) 3 Spec No:1509-1517.
  • LI X, CHANG YH: Amino-terminal protein processing in Saccharomyces cerevisiae is an essential function that requires two distinct methionine aminopepti-dases. Proc. Natl. Acad. ScL USA (1995) 92:12357–12361.
  • GRIFFITH EC, SU Z, TURK BE et al.: Methionineaminopeptidase (type 2) is the common target for angiogenesis inhibitors AGM-1470 and ovalicin. Chem. Biol. (1997) 4:461–471.
  • SIN N, MENG L, WANG MQ, WEN JJ, BORNMANN WG, CREWS CM: The anti-angiogenic agent fumagillin covalently binds and inhibits the methionine aminopeptidase, MetAP-2. Proc. Nati Acad. Sci. USA (1997) 94:6099–6103.
  • GUTHRIE C, FINK GR (Eds.): Guide to yeast genetics and molecular biology. New York: Academic Press (1991).
  • •An excellent theoretical and practical guide for working with Saccharomyces cerevisiae.
  • BAUDIN A, OZIER-KALOGEROPOULOS O, DENOUEL A, LACROUTE F, CULLIN C: A simple and efficient method for direct gene deletion in Saccharomyces cerevisiae. Nucl. Acids Res. (1993) 21:3329–3330.
  • ROTHSTEIN R: Targeting, disruption, replacement and allele rescue: integrative DNA transformation in yeast. Methods Enzymol. (1991) 194:281–301.
  • HUGHES TR, ROBERTS CJ, DAI H et al.: Widespread aneuploidy revealed by DNA microarray expression profiling. Nature Genetics (2000) 25:333–337.
  • WINZELER EA, SHOEMAKER DD, ASTROMOFF A et al: Functional characterization of the S. cerevisiae genome by gene deletion and parallel analysis. Science (1999) 285:901–906.
  • •The use of DNA microarrays and deletion strains for the phenotypic analysis of Saccharomyces cerevisiae.
  • GAUSE GF, LAIKO AV: Yeast mutants with distorted cellmembranes as a detection system for antitumor antibi-otics. Antibiot. Chemother. (1978) 23:21–25.
  • NITISS J, WANG JC: DNA topoisomerase-targetingantitumor drugs can be studied in yeast. Proc. Natl. Acad. Sci. USA (1988) 85:7501–7505.
  • •Pioneering study of topoisomerase I and II poisons in yeast.
  • MCCAMMON MT, HARTMANN MA, BOTTEMA CD, PARKS LW: Sterol methylation in Saccharomyces cerevisiae. Bacteriol (1984) 157:475–483.
  • GABER RF, COPPLE DM, KENNEDY BK, VIDAL M, BARD M: The yeast gene ERG6 is required for normal membrane function but is not essential for biosyn-thesis of the cell-cycle-sparking sterol. Mol Cell. Biol. (1989) 9:3447–3456.
  • HEMENWAY CS, HEITMAN J: Immunosuppressant target protein FKBP12 is required for P-glycoprotein function in yeast. J Biol. Chem. (1996) 271:18527–18534.
  • BALZI E, GOFFEAU A: Yeast multidrug resistance: the PDR network. J. Bioenerget. Biomembr. (1995) 27:71–76.
  • KOLACZKOWSKI M, VAN DER REST M, CYBULARZ-KOLACZKOWSKA A, SOUMILLION JP, KONINGS WN, GOFFEAU A: Anticancer drugs, ionophoric peptides and steroids as substrates of the yeast multidrug transporter Pdr5p. Biol Chem. (1996) 271:31543–31548.
  • BOGUSLAWSKI G. Effects of polymyxin B sulfate and polymyxin B nonapeptide on growth and permeability of the yeast Saccharomyces cerevisiae. Mol. Gen. Genet. (1985) 199:401–405.
  • KELLER BA, PATEL S, FISHER LM: Molecular cloning and expression of the Candida albicans TOP2 gene allows study of fungal DNA topoisomerase II inhibitors in yeast. Biochem. J (1997) 324:329–339.
  • HAMMONDS TR, MAXWELL A, JENKINS JR: Use of a rapid throughput in vivo screen to investigate inhibitors of eukaryo tic top oisomerase II enzymes. Antimicrob. Agents Chemother. (1998) 42:889–894.
  • XIAO W, DERFLER B, CHEN J, SAMSON L: Primary sequence and biological functions of a Saccharomyces cerevisiae 06-m ethylg-uan in e /04-m ethylthymin e DNA repair methyltransferase gene. EMBO J. (1991) 10:2179–2186.
  • DUNSTAN HM, LUDLOW C, GOEHLE S et al.: Cell based assays for the identification of selectively toxic compounds: novel DSB inducing compounds. (submitted).
  • DEVITO SC, STEPHANI RA: Synthesis and pharmacol- ogicalevaluationofsomenovel13 4N,N-dialkylamino -alkyliben zo [g][2]benzopyrano [4,3-b]indo1-5[1311]ones. Med. Chem. Res. (1991) 1:47–51.
  • JEGGO PA: Identification of genes involved in repair of DNA double-strand breaks in mammalian cells. Rad. Res. (1998) 150:S80–91.
  • JEGGO PA: DNA breakage and repair. Adv. Genetics (1998) 38:185–218.
  • BUOLAMWINI JK: Novel anticancer drug discovery. Curr. Opin. Chem. Biol. (1999) 3:500–509.
  • GIBBS JB: Mechanism-based target identification and drug discovery in cancer research. Science (2000) 287:1969–1973.
  • SHERR CJ: Cancer cell cycles. Science (1996) 274:1672–1677.
  • SHERR CJ: The Pezcoller lecture: cancer cell cycles revisited. Cancer Res. (2000) 60:3689–3695.
  • MOORTHAMER M, PANCHAL M, GREENHALF W, CHAUDHURI B: The p16(INK4A) protein and flavopiridol restore yeast cell growth inhibited by Cdk4. Biochem. Biophys. Res. Commun. (1998) 250:791–797.
  • •A report showing that expression of human Cdk4 in yeast leads to a kinase-dependent cell cycle arrest. The authors also demonstrate that co-expression of the cdk inhibitor pl6INK4A blocks this arrest.
  • LORCH Y, KORNBERG RD: A region flanking the GAL7 gene and a binding site for GALA protein as upstream activating sequences in yeast. J. Mol. Biol. (1985) 186:821–824.
  • JOHNSTON M: A model fungal gene regulatory mechanism: the GAL genes of Saccharomyces cerevisiae. Microbic)]. Rev. (1987) 51:458–476.
  • NASMYTH KA, REED SI: Isolation of genes by comple-mentation in yeast: molecular cloning of a cell-cycle gene. Proc. Natl. Acad. Sci. USA (1980) 77:2119–2213.
  • TIMBLIN BK, TATCHELL K, BERGMAN LW: Deletion ofthe gene encoding the cyclin-dependent protein kinase Pho85 alters glycogen metabolism in Saccha-romyces cerevisiae. Genetics (1996) 143:57–66.
  • BALCIUNAS D, RONNE H: Three subunits of the RNApolymerase II mediator complex are involved in glucose repression. Nucl. AcidsRes. (1995) 23:4421–4425.
  • LEE JM, GREENLEAF AL: CTD kinase large subunit isencoded by CTK1, a gene required for normal growth of Saccharomyces cerevisiae. Gene Expr. (1991) 1:149–167.
  • VALAY JG, SIMON M, FAYE G: The kin28 protein kinaseis associated with a cyclin in Saccharomyces cerevisiae. j Mol Biol. (1993) 23 4:307–310.
  • KELEKAR A, THOMPSON CB: Bc1-2-family proteins: therole of the BH3 domain in apoptosis. Trends Cell Biol. (1998) 8:324–330.
  • DECAUDIN D, GELEY S, HIRSCH T et al: Bc1-2 and Bc1-XLantagonize the mitochondrial dysfunction preceding nuclear apoptosis induced by chemotherapeutic agents. Cancer Res. (1997) 57:62–67.
  • TAO W, KURSCHNER C, MORGAN JI: Bc1-xS and Badpotentiate the death suppressing activities of Bc1-xL, Bc1-2 and Al in yeast. J Biol. Chem. (1998) 273:23704–23708.
  • XU Q, JURGENSMEIER JM, REED JC: Methods of assayingBc1-2 and Bax family proteins in yeast. Methods (1999) 17:292–304.
  • •A detailed review of the experimental techniques required for analysis of Bc12 and Box function in Saccharomyces cerevisiae and Schizosaccharomyces pombe.
  • HOYT MA, HE L, TOTIS L, SAUNDERS WS: loss offunction of Saccharomyces cerevisiae kinesin-r elated CMS and KIP1 is suppressed by KÁR3motor domain mutations. Genetics (1993) 135:35–44.
  • HOYT MA, TOTIS L, ROBERTS BT: S. cerevisiae genesrequired for cell cycle arrest in response to loss of microtubule function. Cell (1991) 66:507–517.
  • HILDEBRANDT ER, HOYT MA: Mitotic motors in Saccha-romyces cerevisiae. Biochim. Biophys. Acta (2000) 1496:99–116.
  • STRAIGHT AF, SEDAT JW, MURRAY AW: Time-lapse microscopy reveals unique roles for kinesins during anaphase in budding yeast. J. Cell Biol. (1998) 143:687–694.
  • STRAIGHT AF, MURRAY AW: The spindle assembly checkpoint in budding yeast. Methods Enzymol. (1997) 283:425–440.
  • LI R, MURRAY AW: Feedback control of mitosis inbudding yeast. Cell (1991) 66:519–531.
  • HARDWICK KG, LI R, MISTROT C et al.: lesions in manydifferent spindle components activate the spindle checkpoint in the budding yeast Saccharomyces cerevisiae. Genetics (1999) 152:509–518.
  • CAHILL DP, LENGAUER C, YU J et al.: Mutations ofmitotic checkpoint genes in human cancers. Nature (1998) 392:300–303.
  • •Identification of specific mutations in human colon carcinoma cell lines that interfere with the function of the mitotic spindle assembly checkpoint and potentially are responsible for aneuploidy.
  • PARSONS R, LI GM, LONGLEY MJ et al: Hypermutabilityand mismatch repair deficiency in REle tumor cells. Cell (1993) 75:1227–1236.
  • FUJI WARA T, STOLKER JM, WATANABE T et al.: Accumu-lated clonal genetic alterations in familial and sporadic colorectal carcinomas with widespread instability in microsatellite sequences. Am. J Path. (1998) 153:1063–1078.
  • KROLL E, THORNTON B, DASHIELL M, FRIEND S: lesions in DNA p olymerases and ribonucleotide reductase are synthetically lethal with mismatch repair. submitted.
  • ELLEDGE SJ, DAVIS RW: Two genes differentially regulated in the cell cycle and by DNA-damaging agents encode alternative regulatory subunits of ribonucleotide reductase. Genes & Devel. (1990) 4:740–751.
  • PRICE C, NASMYTH K, SCHUSTER T: A gen eral approach to the isolation of cell cycle-regulated genes in the budding yeast, Saccharomyces cerevisiae. J. Mol. (1991) 218:543–556.
  • MITCHISON TJ: Towards a pharmacological genetics. Chem. Biol. (1994) 1:3–6.
  • •A perspective on the potential of combining classic genetics, chemical synthetis and pharmacology in an integrated drug discovery program.
  • SCHREIBER SL: Chemical genetics resulting from a passion for synthetic organic chemistry. Bioorg. Med. Chem. (1998) 6:1127–1152.
  • •A scientist's personal prespective on the application of chemistry and chemical synthesis in the study of biological systems.
  • RICHARDSON HE, WITTENBERG C, CROSS F, REED SI: An essential G1 function for cyclin-like proteins in yeast. Cell (1989) 59:1127–1133.
  • REED SI, DULIC V, LEW DJ, RICHARDSON HE, WITTEN-BERG C: G1 control in yeast and animal cells. Ciba Found. Symp. (1992) 170:7-15 (discussion 15–9).
  • DELSAL G, LODA M, PAGANO M: Cell cycle and cancer: critical events at the G1 restriction point. Crit. Rev. Oncogen. (1996) 7:127–142.
  • FUNK JO: Cancer cell cycle control. AntiCancer Res. (1999) 19:4772–4780.
  • YUSTE-ROJAS M, CROSS FR: Mutations in CDC14 resultin high sensitivity to cyclin gene dosage in Saccharo-myces cerevisiae. Mol. Gen. Genet. (2000) 263:60–72.
  • WEINERT TA, KISER GL, HARTWELL LH: Mitoticcheckpoint genes in budding yeast and the depend-ence of mitosis on DNA replication and repair. Genes Devel (1994) 8:652–665.
  • KISER GL, WEINERT TA: Distinct roles of yeast MEC and RAD checkpoint genes in transcriptional induction after DNA damage and implications for function. Mol. Biol. Cell (1996) 7:703–718.
  • VISINTIN R, CRAIG K, HVVANG ES, PRINZ S, TYERS M, AMON A: The phosphatase Cdc14 triggers mitotic exit by reversal of Cdk-dependent phosphorylation. Mol. Cell (1998) 2:709–718.
  • MARELLI M, AITCHISON JD, WOZNIAK RW: Specific binding of the karyopherin Kap12Ip to a subunit of the nuclear pore complex containing Nup53p, Nup59p and Nup170p. J. Cell Biol. (1998) 143:1813–1830.
  • RINE J, HANSEN W, HARDEMAN E, DAVIS RW: Targeted selection of recombinant clones through gene dosage effects. Proc. Natl. Acad. ScL USA (1983) 80:6750–6754.
  • ••Initial demonstration of dosage effects in drug sensitivity asa method for target identification in yeast. The authors demonstrate that resistance to three agents, tunicamycin, compactin and ethionine can be realised by transforming wild type yeast with plasmid-encoded yeast genes.
  • BARNES G, HANSEN WJ, HOLCOMB CL, RINE J: Asp ar agine-linked glycosylation in Saccharomyces cerevisiae: genetic analysis of an early step. Mol. Biol. (1984) 4:2381–2388.
  • •An example of a classic, genetic approach for the identifica-tion of drug.
  • ISHIDA R, HAMATAKE M, WASSERMAN RA, NITISS JL, WANG JC, ANDOH T: DNA topoisomerase II is the molecular target of bisdioxopiperazine derivatives ICRF-159 and ICRF-193 in Saccharomyces cerevisiae. Cancer Res. (1995) 55:2299–2303.
  • GIAEVER G, SHOEMAKER DD, JONES TVV et al: Genomic profiling of drug sensitivities via induced haploinsuf-ficiency. Nature Genet. (1999) 21:278–283.
  • ••A demonstration of a genome-wide method for target identi-fication in yeast. Using heterozygous diploid deletion yeast strains, the authors are able to detect a growth disadvantage for strains grown in the presence of a drug that targets the protein encoded by the deleted open reading frame.
  • LICITRA EJ, LIU JO: A three-hybrid system for detecting small ligand-protein receptor interactions. Proc. Natl. Acad. ScL USA (1996) 93:12817–12821.
  • •Adaptation of the yeast two-hybrid system for drug target identification using the immunosuppressant FK506.
  • HUANG J, SCHREIBER SL: A yeast genetic system for selecting small molecule inhibitors of protein-protein interactions in nanodroplets. PNAS (1997) 94:13396–13401.
  • YOUNG K, LIN S, SUN L et al: Identification of a calcium channel modulator using a high throughpur yeast two-hybrid screen. Nature Biotech. (1998) 16:946–950.
  • •An example of using the yeast two-hybrid system to identify small molecules that disrupt protein/protein interactions.
  • CHIU MI, KATZ H, BERLIN V: RAPT!, a mammalian homologue of yeast Tor, interacts with the FKBP12/rapamycin complex. Proc. Natl. Acad. Sci. USA (1994) 91 :12574–12578.
  • •An application of the yeast two-hybrid system for the identi-fication of the mammalian target of rapamycin (FRAP, mTOR, RAPT, RAFT). An example of a drug that promotes protein/protein complex formation.

Websites

  • http://genome-www.stanford.edu/Saccharomyces/ CHERRY JM, BALL C, DOLINSKI K et al.: Saccharomyces Genome Database.
  • http://dtp.nci.nih.gov EVANS DRH, SZANKASI P, DUNSTAN HM et al.: Follow links to Public Data and NCI Yeast Anticancer Drug Screen

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