27
Views
65
CrossRef citations to date
0
Altmetric
DNA Dynamics and Chromosome Structure

Gene Amplification in a p53-Deficient Cell Line Requires Cell Cycle Progression under Conditions That Generate DNA Breakage

, , &
Pages 3089-3100 | Received 26 Sep 1997, Accepted 06 Feb 1998, Published online: 28 Mar 2023

REFERENCES

  • Almasan, A., S. P. Linke, T. G. Paulson, L. Huang, and G. M. Wahl 1995. Genetic instability as a consequence of inappropriate entry into and progression through S-phase. Cancer Metas. Rev. 14: 59–73.
  • Almasan, A., Y. Yin, R. Kelly, E. Lee, A. Bradley, W. Li, J. Bertino, and G. Wahl 1995. pRb deficiency leads to inappropriate entry into S-phase, activation of E2F responsive genes and apoptosis. Proc. Natl. Acad. Sci. USA 92: 5436–5440.
  • Anderson, M. J., C. L. Fasching, H. J. Xu, W. F. Benedict, and E. J. Stanbridge 1994. Chromosome 13 transfer provides evidence for regulation of RB1 protein expression. Genes Chromosomes Cancer 9: 251–260.
  • Andrulis, I. L., R. Argonza, and A. E. Cairney 1990. Molecular and genetic characterization of human cell lines resistant to l-asparaginase and albizziin. Somat. Cell Mol. Genet. 16: 59–65.
  • Ausubel, F. M., R. Brent, R. E. Kingston, D. D. Moore, J. G. Seidman, J. A. Smith, and K. Struhl 1994. One-dimensional gel electrophoresis of proteins, 10.2. Current protocols in molecular biology. In: Jannsen, K. Wiley-Interscience, New York, N.Y.
  • Ayusawa, D., K. Shimizu, H. Koyama, K. Takeishi, and T. Seno 1983. Accumulation of DNA strand breaks during thymineless death in thymidylate synthase-negative mutants of mouse FM3A cells. J. Biol. Chem. 258: 12448–12454.
  • Benner, S. E., G. M. Wahl, and H. D. Von 1991. Double minute chromosomes and homogeneously staining regions in tumors taken directly from patients versus in human tumor cell lines. Anticancer Drugs 2: 11–25.
  • Boveri, T. 1929. (trans.) The origin of malignant tumours. Williams and Wilkins, Baltimore, Md.
  • Brown, P. C., T. D. Tlsty, and R. T. Schimke 1983. Enhancement of methotrexate resistance and dihydrofolate reductase gene amplification by treatment of mouse 3T6 cells with hydroxyurea. Mol. Cell. Biol. 3: 1097–1107.
  • Chen, C., I. Hall, T. Lansing, T. Gilmer, and M. Kastan 1996. Separate pathways for p53 induction by ionizing radiation and N-(Phosphonoacetyl)-l aspartate. Cancer Res. 56: 3659–3662.
  • Chen, T. R. 1977. In situ detection of mycoplasma contamination in cell cultures by fluorescent Hoechst 33258 stain. Exp. Cell Res. 104: 255–262.
  • Chen, Y., B. Goz, and L. Kirkman 1993. An analysis of vincristine-resistance in BHK cells pretreated with 1-beta-d-arabinofuranosylcytosine. Anticancer Res. 13: 249–255.
  • Coquelle, A., E. Pipiras, F. Toledo, G. Buttin, and M. Debatisse 1997. Expression of fragile sites triggers intrachromosomal mammalian gene amplification and sets boundaries to early amplicons. Cell 89: 215–225.
  • Cowell, J. K., and O. J. Miller 1983. Occurrence and evolution of homogeneously staining regions may be due to breakage-fusion-bridge cycles following telomere loss. Chromosoma 88: 216–221.
  • Cross, S. M., C. A. Sanchez, C. A. Morgan, M. K. Schimke, S. Ramel, R. L. Idzerda, W. H. Raskind, and B. J. Reid 1995. A p53-dependent mouse spindle checkpoint. Science 267: 1353–6.
  • DeGregori, J., T. Kowalik, and J. R. Nevins 1995. Cellular targets for activation by the E2F1 transcription factor include DNA synthesis- and G1/S-regulatory genes. Mol. Cell. Biol. 15: 4215–4224.
  • Denko, N., J. Stringer, M. Wani, and P. Stambrook 1995. Mitotic and post mitotic consequences of genomic instability induced by oncogenic Ha-ras. Somat. Cell Mol. Genet. 21: 241–253.
  • Denko, N. C., A. J. Giaccia, J. R. Stringer, and P. J. Stambrook 1994. The human Ha-ras oncogene induces genomic instability in murine fibroblasts within one cell cycle. Proc. Natl. Acad. Sci. USA 91: 5124–5128.
  • de Vries, J. E., F. H. Kornips, P. Marx, F. T. Bosman, J. P. Geraedts, and J. ten Kate 1993. Transfected c-Ha-ras oncogene enhances karyotypic instability and integrates predominantly in aberrant chromosomes. Cancer Genet. Cytogenet. 67: 35–43.
  • Di Leonardo, A., P. Cavolina, and A. Maddalena 1993. DNA topoisomerase II inhibition and gene amplification in V79/B7 cells. Mutat. Res. 301: 177–182.
  • Di Leonardo, A., S. H. Khan, S. P. Linke, V. Greco, G. Seidita, and G. M. Wahl 1997. DNA rereplication in the presence of mitotic spindle inhibitors in human and mouse fibroblasts lacking either p53 or pRb function. Cancer Res. 57: 1013–1019.
  • Di Leonardo, A., S. P. Linke, K. Clarkin, and G. M. Wahl 1994. DNA damage triggers a prolonged p53-dependent G1 arrest and long-term induction of Cip1 in normal human fibroblasts. Genes Dev. 8: 2540–2551.
  • Di Leonardo, A., S. P. Linke, Y. Yin, and G. M. Wahl 1993. Cell cycle regulation of gene amplification. Cold Spring Harbor Symp. Quant. Biol. 58: 655–667.
  • Flintoff, W. F., S. V. Davidson, and L. Siminovitch 1976. Isolation and partial characterization of three methotrexate-resistant phenotypes from Chinese hamster ovary cells. Somat. Cell Genet. 2: 245–261.
  • Frei, E., A. Rosowsky, J. E. Wright, C. A. Cucchi, J. A. Lippke, T. J. Ervin, J. Jolivet, and W. A. Haseltine 1984. Development of methotrexate resistance in a human squamous cell carcinoma of the head and neck in culture. Proc. Natl. Acad. Sci. USA 81: 2873–2877.
  • Fukasawa, K., and G. F. Vande Woude 1997. Synergy between the Mos/mitogen-activated protein kinase pathway and loss of p53 function in transformation and chromosome instability. Mol. Cell. Biol. 17: 506–518.
  • Greenblatt, M. S., W. P. Bennett, M. Hollstein, and C. C. Harris 1994. Mutations in the p53 tumor suppressor gene: clues to cancer etiology and molecular pathogenesis. Cancer Res. 54: 4855–4878.
  • Hahn, P. J. 1993. Molecular biology of double-minute chromosomes. Bioessays 15: 477–484.
  • Hartwell, L. H., and M. B. Kastan 1994. Cell cycle control and cancer. Science 266: 1821–1828.
  • Hill, A., and R. Schimke 1985. Increased gene amplification in L5178Y mouse lymphoma cells with hydroxyurea-induced chromosomal aberrations. Cancer Res. 45: 5050–5057.
  • Huang, L.-C., K. C. Clarkin, and G. M. Wahl 1996. Sensitivity and selectivity of the p53-mediated DNA damage sensor. Proc. Natl. Acad. Sci. USA 93: 4827–4832.
  • Hundley, J. E., S. K. Koester, D. A. Troyer, S. G. Hilsenbeck, M. A. Subler, and J. J. Windle 1997. Increased tumor proliferation and genomic instability without decreased apoptosis in MMTV-ras mice deficient in p53. Mol. Cell. Biol. 17: 723–731.
  • Johnson, B. E., J. Battey, I. Linnoila, K. L. Becker, R. W. Makuch, R. H. Snider, D. N. Carney, and J. D. Minna 1986. Changes in the phenotype of human small cell lung cancer cell lines after transfection and expression of the c-myc proto-oncogene. J. Clin. Invest. 78: 525–32.
  • Johnson, D. G., J. K. Schwarz, W. D. Cress, and J. R. Nevins 1993. Expression of transcription factor E2F1 induces quiescent cells to enter S phase. Nature 365: 349–352.
  • Johnston, R., S. Beverley, and R. Schimke 1983. Rapid spontaneous dihydrofolate reductase gene amplification shown by fluorescence-activated cell sorting. Proc. Natl. Acad. Sci. USA 80: 3711–3715.
  • Kastan, M. B., Q. Zhan, W. S. El-Deiry, F. Carrier, T. Jacks, W. V. Walsh, B. S. Plunkett, B. Vogelstein, and A. J. Fornace 1992. A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia. Cell 71: 587–597.
  • Kuerbitz, S. J., B. S. Plunkett, W. V. Walsh, and M. B. Kastan 1992. Wild-type p53 is a cell cycle checkpoint determinant following irradiation. Proc. Natl. Acad. Sci. USA 89: 7491–7495.
  • Kufe, D. W., J. D. Griffin, and D. R. Spriggs. 1985. Cellular and clinical pharmacology of low-dose ara-C. Semin. Oncol. 2(Suppl. 3):200–207.
  • Kuo, M. T., R. C. Vyas, L. X. Jiang, and W. N. Hittelman 1994. Chromosome breakage at a major fragile site associated with P-glycoprotein gene amplification in multidrug-resistant CHO cells. Mol. Cell. Biol. 14: 5202–5211.
  • Labrecque, S., and G. J. Matlashewski 1995. Viability of wild type p53-containing and p53-deficient tumor cells following anticancer treatment: the use of human papillomavirus E6 to target p53. Oncogene 11: 387–392.
  • Lee, J. M., and A. Bernstein 1995. Apoptosis, cancer and the p53 tumour suppressor gene. Cancer Metastasis Rev. 14: 149–161.
  • Li, C. Y., H. Nagasawa, W. K. Dahlberg, and J. B. Little 1995. Diminished capacity for p53 in mediating a radiation-induced G1 arrest in established human tumor cell lines. Oncogene 11: 1885–1892.
  • Li, J. C., and E. Kaminskas 1984. Accumulation of DNA strand breaks and methotrexate cytotoxicity. Proc. Natl. Acad. Sci. USA 81: 5694–5698.
  • Li, W., J. Fan, D. Hochhauser, D. Banerjee, Z. Zielinski, A. Almasan, Y. Yin, R. Kelly, G. M. Wahl, and J. R. Bertino 1995. Lack of functional retinoblastoma protein mediates increased resistance to antimetabolites in human sarcoma cell lines. Proc. Natl. Acad. Sci. USA 92: 10436–10440.
  • Linke, S. P., K. C. Clarkin, L. A. Di, A. Tsou, and G. M. Wahl 1996. A reversible, p53-dependent G0/G1 cell cycle arrest induced by ribonucleotide depletion in the absence of detectable DNA damage. Genes Dev. 10: 934–947.
  • Little, J. B., H. Nagasawa, P. C. Keng, Y. Yu, and C. Y. Li 1995. Absence of radiation-induced G1 arrest in two closely related human lymphoblast cell lines that differ in p53 status. J. Biol. Chem. 270: 11033–11036.
  • Livingstone, L. R., A. White, J. Sprouse, E. Livanos, T. Jacks, and T. D. Tisty 1992. Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53. Cell 70: 923–935.
  • Ma, C., S. Martin, B. Trask, and J. L. Hamlin 1993. Sister chromatid fusion initiates amplification of the dihydrofolate reductase gene in Chinese hamster cells. Genes Dev. 7: 605–620.
  • Marder, B. A., and W. F. Morgan 1993. Delayed chromosomal instability induced by DNA damage. Mol. Cell. Biol. 13: 6667–6677.
  • McClintock, B. 1984. The significance of responses of the genome to challenge. Science 226: 792–801.
  • Moran, R. G., M. Mulkins, and C. Heidelberger 1979. Role of thymidylate synthetase activity in development of methotrexate cytotoxicity. Proc. Natl. Acad. Sci. USA 76: 5924–5928.
  • Moyer, J. D., P. A. Smith, E. J. Levy, and R. E. Handschumacher 1982. Kinetics of N-(phosphonacetyl)-l-aspartate and pyrazofurin depletion of pyrimidine ribonucleotide and deoxyribonucleotide pools and their relationship to nucleic acid synthesis in intact and permeabilized cells. Cancer Res. 42: 4525–4531.
  • Nagasawa, H., C. Y. Li, C. G. Maki, A. C. Imrich, and J. B. Little 1995. Relationship between radiation-induced G1 phase arrest and p53 function in human tumor cells. Cancer Res. 55: 1842–1846.
  • Nelson, W. G., and M. B. Kastan 1994. DNA strand breaks: the DNA template alterations that trigger p53-dependent DNA damage response pathways. Mol. Cell. Biol. 14: 1815–1823.
  • Nelson, W. G., and M. B. Kastan 1994. DNA strand breaks: the DNA template alterations that trigger p53-dependent DNA damage response pathways. Mol. Cell. Biol. 14: 1815–1823.
  • Paulovich, A. G., D. P. Toczyski, and L. H. Hartwell 1997. When checkpoints fail. Cell 88: 315–321.
  • Poupon, M. F., K. A. Smith, O. B. Chernova, C. Gilbert, and G. R. Stark 1996. Inefficient growth arrest in response to dNTP starvation stimulates gene amplification through bridge-breakage-fusion cycles. Mol. Biol. Cell 7: 345–354.
  • Rasheed, S. 1974. Characterization of a newly derived human sarcoma cell line (HT-1080). Cancer 33: 1027–1033.
  • Ruiz, J. C., and G. M. Wahl 1990. Chromosomal destabilization during gene amplification. Mol. Cell. Biol. 10: 3056–3066.
  • Scheffner, M., B. A. Werness, J. M. Huibregtse, A. J. Levine, and P. M. Howley 1990. The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53. Cell 63: 1129–1136.
  • Schimke, R. T. 1988. Gene amplification in cultured cells. J. Biol. Chem. 263: 5989–5992.
  • Schimke, R. T. 1992. Gene amplification; what are we learning? Mutat. Res. 276: 145–149.
  • Seeger, R. C., G. M. Brodeur, H. Sather, A. Dalton, S. E. Siegel, K. Y. Wong, and D. Hammond 1985. Association of multiple copies of the N-myc oncogene with rapid progression of neuroblastomas. N. Engl. J. Med. 313: 1111–1116.
  • Sharma, R. C., and R. T. Schimke 1989. Enhancement of the frequency of methotrexate resistance by G-radiation in Chinese hamster ovary and mouse 3T6 cells. Cancer Res. 49: 3861–3866.
  • Sherr, C. J. 1996. Cancer cell cycles. Science 274: 1672–1677.
  • Slamon, D. J., W. Godolphin, L. A. Jones, J. A. Holt, S. G. Wong, D. E. Keith, W. J. Levin, S. G. Stuart, J. Udove, A. Ullrich, and M. Press 1989. Studies of the HER-2/neu proto-oncogene in human breast and ovarian cancer. Science 244: 707–712.
  • Smith, K. A., M. L. Agarwal, M. V. Chernov, O. B. Chernova, Y. Deguchi, Y. Ishizaka, T. E. Patterson, M. F. Poupon, and G. R. Stark 1995. Regulation and mechanisms of gene amplification. Philos. Trans. R. Soc. London B 347: 49–56.
  • Smith, K. A., O. B. Chernova, R. P. Groves, M. B. Stark, J. L. Martinez, J. N. Davidson, J. M. Trent, T. E. Patterson, A. Agarwal, P. Duncan, M. L. Agarwal, and G. R. Stark 1997. Multiple mechanisms of N-phosphonacetyl-l-aspartate resistance in human cell lines: carbamyl-P synthetase/aspartate transcarbamylase/dihydro-orotase gene amplification is frequent only when chromosome 2 is rearranged. Proc. Natl. Acad. Sci. USA 94: 1816–1821.
  • Smith, K. A., M. B. Stark, P. A. Gorman, and G. R. Stark 1992. Fusions near telomeres occur very early in the amplification of CAD genes in Syrian hamster cells. Proc. Natl. Acad. Sci. USA 89: 5427–5431.
  • Sullivan, N. F., R. W. Sweet, M. Rosenberg, and J. R. Feramisco. 1986. Microinjection of the ras oncogene protein into nonestablished rat embryo fibroblasts. Cancer Res.: 6427–6432.
  • Swyryd, E. A., S. S. Seaver, and G. R. Stark 1974. N-(Phosphonacetyl)-l-aspartate, a potent transition state analog inhibitor of aspartate transcarbamylase, blocks proliferation of mammalian cells in culture. J. Biol. Chem. 249: 6945–6950.
  • Tlsty, T., P. C. Brown, R. Johnston, and R. T. Schimke 1982. Enhanced frequency of generation of methotrexate resistance and gene amplification in cultured mouse and hamster cell lines Gene amplification. In: Schimke, R. T.231–238Cold Spring Harbor Laboratory, Cold Spring Harbor, N.Y.
  • Tlsty, T. D. 1990. Normal diploid human and rodent cells lack a detectable frequency of gene amplification. Proc. Natl. Acad. Sci. USA 87: 3132–3136.
  • Tlsty, T. D., B. H. Margolin, and K. Lum 1989. Differences in the rates of gene amplification in nontumorigenic and tumorigenic cell lines as measured by Luria-Delbruck fluctuation analysis. Proc. Natl. Acad. Sci. USA 86: 9441–9445.
  • Varshavsky, A. 1981. Phorbol ester dramatically increases incidence of methotrexate-resistant mouse cells: possible mechanisms and relevance to tumor promotion. Cell 25: 561–572.
  • Wahl, G., P. Gaudray, S. Carroll, and N. Proctor 1986. Is gene amplification inducible? Cancer frontiers, proceedings of the Second International Conference on Progress in Cancer Research. In: Dulbecco, R., V. De Vita, L. Santi, and L. Zardi71–98Humana Press, Totowa, N.J.
  • Werness, B. A., A. J. Levine, and P. M. Howley 1990. Association of human papillomavirus types 16 and 18 E6 proteins with p53. Science 248: 76–79.
  • Wettergren, Y., A. Kullberg, and G. Levan 1994. Drug-specific rearrangements of chromosome 12 in hydroxyurea-resistant mouse SEWA cells: support for chromosomal breakage model of gene amplification. Somat. Cell Mol. Genet. 20: 267–285.
  • White, A. E., E. M. Livanos, and T. D. Tlsty 1994. Differential disruption of genomic integrity and cell cycle regulation in normal human fibroblasts by the HPV oncoproteins. Genes Dev. 8: 666–677.
  • Windle, B., B. W. Draper, Y. X. Yin, S. O’Gorman, and G. M. Wahl 1991. A central role for chromosome breakage in gene amplification, deletion formation, and amplicon integration. Genes Dev. 5: 160–174.
  • Windle, B. E., and G. M. Wahl 1992. Molecular dissection of mammalian gene amplification: new mechanistic insights revealed by analyses of very early events. Mutat. Res. 276: 199–224.
  • Wright, J. A., H. S. Smith, F. M. Watt, M. C. Hancock, D. L. Hudson, and G. R. Stark 1990. DNA amplification is rare in normal human cells. Proc. Natl. Acad. Sci. USA 87: 1791–1795.
  • Wu, X., and A. J. Levine 1994. p53 and E2F-1 cooperate to mediate apoptosis. Proc. Natl. Acad. Sci. USA 91: 3602–3606.
  • Yang, J. K., J. N. Masters, and G. Attardi 1984. Human dihydrofolate reductase gene organization. Extensive conservation of the G + C-rich 5′ non-coding sequence and strong intron size divergence from homologous mammalian genes. J. Mol. Biol. 176: 169–187.
  • Yin, Y., M. A. Tainsky, F. Z. Bischoff, L. C. Strong, and G. M. Wahl 1992. Wild-type p53 restores cell cycle control and inhibits gene amplification in cells with mutant p53 alleles. Cell 70: 937–948.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.