The interaction of cisplatin with a human telomeric DNA sequence containing seventeen tandem repeats.

The anti-tumour drug, cisplatin, preferentially forms adducts at G-rich DNA sequences. Telomeres are found at the ends of chromosomes and, in humans, contain the repeated DNA sequence (GGGTTA)(n) that is expected to be targeted by cisplatin. Using a plasmid clone with 17 tandem telomeric repeats, (GGGTTA)(17), the DNA sequence specificity of cisplatin was investigated utilising the linear amplification procedure that pin-pointed the precise sites of cisplatin adduct formation. This procedure used a fluorescently labelled primer and capillary electrophoresis with laser-induced fluorescence detection to determine the DNA sequence specificity of cisplatin. This technique provided a very accurate analysis of cisplatin-DNA adduct formation in a long telomeric repeat DNA sequence. The DNA sequence specificity of cisplatin in a long telomeric tandem repeat has not been previously reported. The results indicated that the 3'-end of the G-rich strand of the telomeric repeat was preferentially damaged by cisplatin and this suggests that the telomeric DNA repeat has an unusual conformation.

[1]  D. Housman,et al.  Isolation and characterization of human cDNA clones encoding a high mobility group box protein that recognizes structural distortions to DNA caused by binding of the anticancer agent cisplatin. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[2]  Bernhard Lippert,et al.  Cisplatin : chemistry and biochemistry of a leading anticancer drug , 2006 .

[3]  D. Phillips,et al.  Sequence-dependent termination of bacteriophage T7 transcription in vitro by DNA-binding drugs. , 1989, Biochemistry.

[4]  K. Riabowol,et al.  Acceleration of Telomere Loss by Chemotherapy Is Greater in Older Patients with Locally Advanced Head and Neck Cancer , 2006, Clinical Cancer Research.

[5]  Julie E Reed,et al.  Stabilisation of human telomeric quadruplex DNA and inhibition of telomerase by a platinum-phenanthroline complex. , 2007, Chemical communications.

[6]  W. Haseltine,et al.  Quantitation of cyclobutane pyrimidine dimer formation in double- and single-stranded DNA fragments of defined sequence. , 1982, Radiation research.

[7]  L. Kèlland,et al.  The resurgence of platinum-based cancer chemotherapy , 2007, Nature Reviews Cancer.

[8]  P. Lobachevsky,et al.  Iodine-125 Decay in a Synthetic Oligodeoxynucleotide. I. Fragment Size Distribution and Evaluation of Breakage Probability , 2000, Radiation research.

[9]  V. Murray,et al.  The sequence specificity of the anti-tumour drug, cisplatin, in telomeric DNA sequences compared with consecutive guanine DNA sequences. , 2012, Anti-cancer agents in medicinal chemistry.

[10]  H. Earl,et al.  Chemotherapy for ovarian cancer--a consensus statement on standard practice. , 1998, British Journal of Cancer.

[11]  K. Comess,et al.  Replication inhibition and translesion synthesis on templates containing site-specifically placed cis-diamminedichloroplatinum(II) DNA adducts. , 1992, Biochemistry.

[12]  R. Souhami,et al.  Measurement of the sequence specificity of covalent DNA modification by antineoplastic agents using Taq DNA polymerase. , 1991, Nucleic acids research.

[13]  S. Lippard,et al.  Telomere loss in cells treated with cisplatin. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[14]  Seth M. Cohen,et al.  Formation of cis-diamminedichloroplatinum(II) 1,2-intrastrand cross-links on DNA is flanking-sequence independent. , 2000, Nucleic acids research.

[15]  S. Balcerzak,et al.  A phase II evaluation of cisplatin in unresectable diffuse malignant mesothelioma: A Southwest Oncology Group Study , 1988, Investigational New Drugs.

[16]  L. S. Cram,et al.  A highly conserved repetitive DNA sequence, (TTAGGG)n, present at the telomeres of human chromosomes. , 1988, Proceedings of the National Academy of Sciences of the United States of America.

[17]  W. Denny,et al.  The interaction of DNA-targeted 9-aminoacridine-4-carboxamide platinum complexes with DNA in intact human cells. , 2002, Biochimica et biophysica acta.

[18]  M. Cairns,et al.  The DNA sequence selectivity of maltolato-containing cisplatin analogues in purified plasmid DNA and in intact human cells. , 2009, Journal of inorganic biochemistry.

[19]  D. Falconer,et al.  Introduction to Quantitative Genetics. , 1962 .

[20]  T. Nguyen,et al.  The Use of Automated Sequencing Techniques to Investigate the Sequence Selectivity of DNA‐Damaging Agents , 2012, Chemical biology & drug design.

[21]  S. Lippard,et al.  Structure, Recognition, and Processing of Cisplatin-DNA Adducts. , 1999, Chemical reviews.

[22]  M. Cairns,et al.  Substituted 9-aminoacridine-4-carboxamides tethered to platinum(II)diamine complexes: chemistry, cytotoxicity and DNA sequence selectivity. , 2010, Journal of inorganic biochemistry.

[23]  Stephen Neidle,et al.  Targeting G-quadruplexes in gene promoters: a novel anticancer strategy? , 2011, Nature Reviews Drug Discovery.

[24]  H. Tanke,et al.  Heterogeneity in telomere length of human chromosomes. , 1996, Human molecular genetics.

[25]  P. Lohman,et al.  Adducts of the antitumor drug cis-diamminedichloroplatinum(II) with DNA: formation, identification, and quantitation. , 1985, Biochemistry.

[26]  V. Murray,et al.  Use of an automated capillary DNA sequencer to investigate the interaction of cisplatin with telomeric DNA sequences. , 2011, Biomedical chromatography : BMC.

[27]  K. Hiyama Telomeres and Telomerase in Cancer , 2009 .

[28]  W. Haseltine,et al.  Comparison of the cleavage of pyrimidine dimers by the bacteriophage T4 and Micrococcus luteus UV-specific endonucleases. , 1980, The Journal of biological chemistry.

[29]  Stephen J Lippard,et al.  Direct cellular responses to platinum-induced DNA damage. , 2007, Chemical reviews.

[30]  V. Murray,et al.  The sequence selectivity of DNA-targeted 9-aminoacridine cisplatin analogues in a telomere-containing DNA sequence , 2011, JBIC Journal of Biological Inorganic Chemistry.

[31]  W. Mattes,et al.  DNA sequence selectivity of guanine-N7 alkylation by nitrogen mustards. , 1986, Nucleic acids research.

[32]  S. Lippard,et al.  Influence of cisplatin intrastrand crosslinking on the conformation, thermal stability, and energetics of a 20-mer DNA duplex. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[33]  S. Lippard,et al.  NMR solution structure of a DNA dodecamer duplex containing a cis-diammineplatinum(II) d(GpG) intrastrand cross-link, the major adduct of the anticancer drug cisplatin. , 1998, Biochemistry.

[34]  V. Murray A survey of the sequence-specific interaction of damaging agents with DNA: emphasis on antitumor agents. , 1999, Progress in nucleic acid research and molecular biology.

[35]  V. Murray,et al.  Interaction of 11 cisplatin analogues with DNA: characteristic pattern of damage with monofunctional analogues. , 1997, Biochimica et biophysica acta.

[36]  J. Hoffmann,et al.  Conversion of monofunctional DNA adducts of cis-diamminedichloroplatinum (II) to bifunctional lesions. Effect on the in vitro replication of single-stranded DNA by Escherichia coli DNA polymerase I and eukaryotic DNA polymerases alpha. , 1989, The Journal of biological chemistry.

[37]  T. Nguyen,et al.  Human telomeric DNA sequences are a major target for the antitumour drug bleomycin , 2011, JBIC Journal of Biological Inorganic Chemistry.

[38]  W. Denny,et al.  The use of Taq DNA polymerase to determine the sequence specificity of DNA damage caused by cis-diamminedichloroplatinum(II), acridine-tethered platinum(II) diammine complexes or two analogues. , 1992, The Journal of biological chemistry.

[39]  Dong Wang,et al.  Cellular processing of platinum anticancer drugs , 2005, Nature Reviews Drug Discovery.