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The ability of human papillomavirus E6 proteins to target p53 for degradation in vivo correlates with their ability to abrogate actinomycin D-induced growth arrest

Foster, S A, Demers, G W, Etscheid, B G, Galloway, D A·1994·Journal of Virology
DOI 10.1128/jvi.68.9.5698-5705.1994
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Abstract

Functional p53 protein is associated with the ability of cells to arrest in G1 after DNA damage. The E6 protein of cancer-associated human papillomavirus type 16 (HPV-16) binds to p53 and targets its degradation through the ubiquitin pathway. To determine whether the ability of E6 to interact with p53 leads to a disruption of cell cycle control, mutated E6 proteins were tested for p53 binding and p53 degradation targeting in vitro, the ability to reduce intracellular p53 levels in vivo, and the ability to abrogate actinomycin D-induced growth arrest in human keratinocytes. Mutations scattered throughout the amino terminus, either zinc finger or the central region but not the carboxy terminus, severely reduced the ability of E6 to interact with p53. Expression of HPV-16 E6 or mutated E6 proteins that bound and targeted p53 for degradation in vitro sharply reduced the level of intracellular p53 induced by actinomycin D in human keratinocytes. A perfect correlation between the ability of E6 proteins to reduce the level of intracellular p53 and their ability to block actinomycin D-induced cellular growth arrest was observed. These results suggest that interaction with p53 is important for the ability of HPV E6 proteins to circumvent growth arrest.

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  1. Barbosa M. S., Lowy D. R., Schiller J. T. Papillomavirus polypeptides E6 and E7 are zinc-binding proteins. J Virol. 1989 Mar;63(3):1404–1407. doi: 10.1128/jvi.63.3.1404-1407.1989. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI · Paper page
  2. Bargonetti J., Friedman P. N., Kern S. E., Vogelstein B., Prives C. Wild-type but not mutant p53 immunopurified proteins bind to sequences adjacent to the SV40 origin of replication. Cell. 1991 Jun 14;65(6):1083–1091. doi: 10.1016/0092-8674(91)90560-l. [DOI] [PubMed] [Google Scholar] · DOI
  3. Craig R. W., Frankfurt O. S., Sakagami H., Takeda K., Bloch A. Macromolecular and cell cycle effects of different classes of agents inducing the maturation of human myeloblastic leukemia (ML-1) cells. Cancer Res. 1984 Jun;44(6):2421–2429. [PubMed] [Google Scholar]
  4. Crook T., Tidy J. A., Vousden K. H. Degradation of p53 can be targeted by HPV E6 sequences distinct from those required for p53 binding and trans-activation. Cell. 1991 Nov 1;67(3):547–556. doi: 10.1016/0092-8674(91)90529-8. [DOI] [PubMed] [Google Scholar] · DOI
  5. Demers G. W., Foster S. A., Halbert C. L., Galloway D. A. Growth arrest by induction of p53 in DNA damaged keratinocytes is bypassed by human papillomavirus 16 E7. Proc Natl Acad Sci U S A. 1994 May 10;91(10):4382–4386. doi: 10.1073/pnas.91.10.4382. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI · Paper page
  6. Demers G. W., Halbert C. L., Galloway D. A. Elevated wild-type p53 protein levels in human epithelial cell lines immortalized by the human papillomavirus type 16 E7 gene. Virology. 1994 Jan;198(1):169–174. doi: 10.1006/viro.1994.1019. [DOI] [PubMed] [Google Scholar] · DOI
  7. Desaintes C., Hallez S., Van Alphen P., Burny A. Transcriptional activation of several heterologous promoters by the E6 protein of human papillomavirus type 16. J Virol. 1992 Jan;66(1):325–333. doi: 10.1128/jvi.66.1.325-333.1992. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  8. Fields S., Jang S. K. Presence of a potent transcription activating sequence in the p53 protein. Science. 1990 Aug 31;249(4972):1046–1049. doi: 10.1126/science.2144363. [DOI] [PubMed] [Google Scholar] · DOI
  9. Grossman S. R., Laimins L. A. E6 protein of human papillomavirus type 18 binds zinc. Oncogene. 1989 Sep;4(9):1089–1093. [PubMed] [Google Scholar]
  10. Halbert C. L., Demers G. W., Galloway D. A. The E7 gene of human papillomavirus type 16 is sufficient for immortalization of human epithelial cells. J Virol. 1991 Jan;65(1):473–478. doi: 10.1128/jvi.65.1.473-478.1991. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI · Paper page
  11. Harper J. W., Adami G. R., Wei N., Keyomarsi K., Elledge S. J. The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases. Cell. 1993 Nov 19;75(4):805–816. doi: 10.1016/0092-8674(93)90499-g. [DOI] [PubMed] [Google Scholar] · DOI · Paper page
  12. Hartwell L. Defects in a cell cycle checkpoint may be responsible for the genomic instability of cancer cells. Cell. 1992 Nov 13;71(4):543–546. doi: 10.1016/0092-8674(92)90586-2. [DOI] [PubMed] [Google Scholar] · DOI
  13. Hubbert N. L., Sedman S. A., Schiller J. T. Human papillomavirus type 16 E6 increases the degradation rate of p53 in human keratinocytes. J Virol. 1992 Oct;66(10):6237–6241. doi: 10.1128/jvi.66.10.6237-6241.1992. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  14. Huibregtse J. M., Scheffner M., Howley P. M. Cloning and expression of the cDNA for E6-AP, a protein that mediates the interaction of the human papillomavirus E6 oncoprotein with p53. Mol Cell Biol. 1993 Feb;13(2):775–784. doi: 10.1128/mcb.13.2.775-784.1993. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI · Paper page
  15. Kanda T., Watanabe S., Zanma S., Sato H., Furuno A., Yoshiike K. Human papillomavirus type 16 E6 proteins with glycine substitution for cysteine in the metal-binding motif. Virology. 1991 Dec;185(2):536–543. doi: 10.1016/0042-6822(91)90523-e. [DOI] [PubMed] [Google Scholar] · DOI
  16. Kastan M. B., Onyekwere O., Sidransky D., Vogelstein B., Craig R. W. Participation of p53 protein in the cellular response to DNA damage. Cancer Res. 1991 Dec 1;51(23 Pt 1):6304–6311. [PubMed] [Google Scholar]
  17. Kern S. E., Kinzler K. W., Bruskin A., Jarosz D., Friedman P., Prives C., Vogelstein B. Identification of p53 as a sequence-specific DNA-binding protein. Science. 1991 Jun 21;252(5013):1708–1711. doi: 10.1126/science.2047879. [DOI] [PubMed] [Google Scholar] · DOI
  18. Kessis T. D., Slebos R. J., Nelson W. G., Kastan M. B., Plunkett B. S., Han S. M., Lorincz A. T., Hedrick L., Cho K. R. Human papillomavirus 16 E6 expression disrupts the p53-mediated cellular response to DNA damage. Proc Natl Acad Sci U S A. 1993 May 1;90(9):3988–3992. doi: 10.1073/pnas.90.9.3988. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  19. Klingelhutz A. J., Barber S. A., Smith P. P., Dyer K., McDougall J. K. Restoration of telomeres in human papillomavirus-immortalized human anogenital epithelial cells. Mol Cell Biol. 1994 Feb;14(2):961–969. doi: 10.1128/mcb.14.2.961-969.1994. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  20. Kuerbitz S. J., Plunkett B. S., Walsh W. V., Kastan M. B. Wild-type p53 is a cell cycle checkpoint determinant following irradiation. Proc Natl Acad Sci U S A. 1992 Aug 15;89(16):7491–7495. doi: 10.1073/pnas.89.16.7491. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  21. Lechner M. S., Mack D. H., Finicle A. B., Crook T., Vousden K. H., Laimins L. A. Human papillomavirus E6 proteins bind p53 in vivo and abrogate p53-mediated repression of transcription. EMBO J. 1992 Aug;11(8):3045–3052. doi: 10.1002/j.1460-2075.1992.tb05375.x. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  22. Lin D., Shields M. T., Ullrich S. J., Appella E., Mercer W. E. Growth arrest induced by wild-type p53 protein blocks cells prior to or near the restriction point in late G1 phase. Proc Natl Acad Sci U S A. 1992 Oct 1;89(19):9210–9214. doi: 10.1073/pnas.89.19.9210. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI · Paper page
  23. Livingstone L. R., White A., Sprouse J., Livanos E., Jacks T., Tlsty T. D. Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53. Cell. 1992 Sep 18;70(6):923–935. doi: 10.1016/0092-8674(92)90243-6. [DOI] [PubMed] [Google Scholar] · DOI
  24. Malkin D., Li F. P., Strong L. C., Fraumeni J. F., Jr, Nelson C. E., Kim D. H., Kassel J., Gryka M. A., Bischoff F. Z., Tainsky M. A. Germ line p53 mutations in a familial syndrome of breast cancer, sarcomas, and other neoplasms. Science. 1990 Nov 30;250(4985):1233–1238. doi: 10.1126/science.1978757. [DOI] [PubMed] [Google Scholar] · DOI · Paper page
  25. Mann R., Mulligan R. C., Baltimore D. Construction of a retrovirus packaging mutant and its use to produce helper-free defective retrovirus. Cell. 1983 May;33(1):153–159. doi: 10.1016/0092-8674(83)90344-6. [DOI] [PubMed] [Google Scholar] · DOI
  26. Mietz J. A., Unger T., Huibregtse J. M., Howley P. M. The transcriptional transactivation function of wild-type p53 is inhibited by SV40 large T-antigen and by HPV-16 E6 oncoprotein. EMBO J. 1992 Dec;11(13):5013–5020. doi: 10.1002/j.1460-2075.1992.tb05608.x. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  27. Miller A. D., Buttimore C. Redesign of retrovirus packaging cell lines to avoid recombination leading to helper virus production. Mol Cell Biol. 1986 Aug;6(8):2895–2902. doi: 10.1128/mcb.6.8.2895-2902.1986. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  28. Miller A. D., Garcia J. V., von Suhr N., Lynch C. M., Wilson C., Eiden M. V. Construction and properties of retrovirus packaging cells based on gibbon ape leukemia virus. J Virol. 1991 May;65(5):2220–2224. doi: 10.1128/jvi.65.5.2220-2224.1991. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  29. Miller A. D. Retroviral vectors. Curr Top Microbiol Immunol. 1992;158:1–24. doi: 10.1007/978-3-642-75608-5_1. [DOI] [PubMed] [Google Scholar] · DOI
  30. Miller A. D., Rosman G. J. Improved retroviral vectors for gene transfer and expression. Biotechniques. 1989 Oct;7(9):980-2, 984-6, 989-90. [PMC free article] [PubMed] [Google Scholar]
  31. Noda A., Ning Y., Venable S. F., Pereira-Smith O. M., Smith J. R. Cloning of senescent cell-derived inhibitors of DNA synthesis using an expression screen. Exp Cell Res. 1994 Mar;211(1):90–98. doi: 10.1006/excr.1994.1063. [DOI] [PubMed] [Google Scholar] · DOI · Paper page
  32. Raycroft L., Wu H. Y., Lozano G. Transcriptional activation by wild-type but not transforming mutants of the p53 anti-oncogene. Science. 1990 Aug 31;249(4972):1049–1051. doi: 10.1126/science.2144364. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  33. Scheffner M., Huibregtse J. M., Vierstra R. D., Howley P. M. The HPV-16 E6 and E6-AP complex functions as a ubiquitin-protein ligase in the ubiquitination of p53. Cell. 1993 Nov 5;75(3):495–505. doi: 10.1016/0092-8674(93)90384-3. [DOI] [PubMed] [Google Scholar] · DOI · Paper page
  34. Scheffner M., Münger K., Huibregtse J. M., Howley P. M. Targeted degradation of the retinoblastoma protein by human papillomavirus E7-E6 fusion proteins. EMBO J. 1992 Jul;11(7):2425–2431. doi: 10.1002/j.1460-2075.1992.tb05307.x. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  35. Scheffner M., Werness B. A., Huibregtse J. M., Levine A. J., Howley P. M. The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53. Cell. 1990 Dec 21;63(6):1129–1136. doi: 10.1016/0092-8674(90)90409-8. [DOI] [PubMed] [Google Scholar] · DOI · Paper page
  36. Smotkin D., Wettstein F. O. Transcription of human papillomavirus type 16 early genes in a cervical cancer and a cancer-derived cell line and identification of the E7 protein. Proc Natl Acad Sci U S A. 1986 Jul;83(13):4680–4684. doi: 10.1073/pnas.83.13.4680. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  37. Srivastava S., Zou Z. Q., Pirollo K., Blattner W., Chang E. H. Germ-line transmission of a mutated p53 gene in a cancer-prone family with Li-Fraumeni syndrome. Nature. 1990 Dec 20;348(6303):747–749. doi: 10.1038/348747a0. [DOI] [PubMed] [Google Scholar] · DOI
  38. Trask D. K., Muller M. T. Stabilization of type I topoisomerase-DNA covalent complexes by actinomycin D. Proc Natl Acad Sci U S A. 1988 Mar;85(5):1417–1421. doi: 10.1073/pnas.85.5.1417. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  39. Vogelstein B. Cancer. A deadly inheritance. Nature. 1990 Dec 20;348(6303):681–682. doi: 10.1038/348681a0. [DOI] [PubMed] [Google Scholar] · DOI
  40. Wassermann K., Markovits J., Jaxel C., Capranico G., Kohn K. W., Pommier Y. Effects of morpholinyl doxorubicins, doxorubicin, and actinomycin D on mammalian DNA topoisomerases I and II. Mol Pharmacol. 1990 Jul;38(1):38–45. [PubMed] [Google Scholar]
  41. Werness B. A., Levine A. J., Howley P. M. Association of human papillomavirus types 16 and 18 E6 proteins with p53. Science. 1990 Apr 6;248(4951):76–79. doi: 10.1126/science.2157286. [DOI] [PubMed] [Google Scholar] · DOI · Paper page
  42. White R. A., Terry N. H., Meistrich M. L., Calkins D. P. Improved method for computing potential doubling time from flow cytometric data. Cytometry. 1990;11(2):314–317. doi: 10.1002/cyto.990110214. [DOI] [PubMed] [Google Scholar] · DOI
  43. Yin Y., Tainsky M. A., Bischoff F. Z., Strong L. C., Wahl G. M. Wild-type p53 restores cell cycle control and inhibits gene amplification in cells with mutant p53 alleles. Cell. 1992 Sep 18;70(6):937–948. doi: 10.1016/0092-8674(92)90244-7. [DOI] [PubMed] [Google Scholar] el-Deiry W. S., Tokino T., Velculescu V. E., Levy D. B., Parsons R., Trent J. M., Lin D., Mercer W. E., Kinzler K. W., Vogelstein B. WAF1, a potential mediator of p53 tumor suppression. Cell. 1993 Nov 19;75(4):817–825. doi: 10.1016/0092-8674(93)90500-p. [DOI] [PubMed] [Google Scholar] zur Hausen H. Human papillomaviruses in the pathogenesis of anogenital cancer. Virology. 1991 Sep;184(1):9–13. doi: 10.1016/0042-6822(91)90816-t. [DOI] [PubMed] [Google Scholar] · DOI

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Metadata

Authors
Foster, S. A., Demers, G. W., Etscheid, B. G., & Galloway, D. A.
Affiliations
Fred Hutchinson Cancer Research Center, Seattle, Washington 98104.
Venue
Journal of Virology
Publisher
American Society for Microbiology
Published
1994-09
Volume
68
Issue
9
Pages
5698-5705
ISSN
  • 0022-538X
  • 1098-5514
DOI
10.1128/jvi.68.9.5698-5705.1994
Cited by
160
References
3
Language
en
Licence
journals.asm.org/non-commercial-tdm-license (tdm)

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CoChat. (2026). Citation check: The ability of human papillomavirus E6 proteins to target p53 for degradation in vivo correlates with their ability to abrogate actinomycin D-induced growth arrest. https://app.cochat.ai/papers/10.1128/jvi.68.9.5698-5705.1994
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Foster, S. A., Demers, G. W., Etscheid, B. G., & Galloway, D. A. (1994). The ability of human papillomavirus E6 proteins to target p53 for degradation in vivo correlates with their ability to abrogate actinomycin D-induced growth arrest. Journal of Virology. https://doi.org/10.1128/jvi.68.9.5698-5705.1994