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MeSH Review

Human papillomavirus 18

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Disease relevance of Human papillomavirus 18

  • We found that regardless of the HPV type in SiHa (HPV 16+) CaSki (HPV 16+), HeLa (HPV 18+), and UT-DEC-1 (HPV 33+) cell lines, cisplatin, carboplatin, and a novel platinum compound, oxaliplatin, activated a p53 reporter and reduced the HPV E6 mRNA [1].
  • In this study, we have analysed the intracellular distribution of the E6 oncoproteins from the high-risk HPV-18 and the low-risk HPV-11 [2].
  • In the present study, the wild type p53 protein in human fibrosarcoma HT1080 cells were targeted with HPV-18 E6 and the viability of these cells in response to treatment with adriamycin, u.v.-irradiation and gamma-irradiation was examined [3].
  • Both HSV-1 TIF and ICP0 activated HPV-18 expression; however, activation by TIF was observed only in epithelial cells, while ICP0 stimulated expression in a wide variety of cells [4].
  • We have established cell-free replication for the human papillomavirus type 18 (HPV-18) origin of replication (ori)-containing DNA by using purified HPV-18 E1 and E2 gene products expressed as fusion proteins in Escherichia coli [5].

High impact information on Human papillomavirus 18

  • In contrast, the same full-length E2 protein repressed transcription of the HPV-18 E6/E7 P105 promoter [6].
  • We have identified a negative regulatory domain in the HPV-18 promoter which represses the constitutive and TPA-induced AP-1 activity [7].
  • The transcriptional repressor protein YY1, which negatively regulates the P5 promoter, binds to the HPV-18 silencer with high affinity [7].
  • The human papillomavirus type 18 (HPV-18) promoter contains a TPA responsive element (TRE) which confers TPA responsiveness on a heterologous promoter [7].
  • Down-regulation of HPV 18 mRNA correlates directly with cessation of cellular growth and can be abolished using the protein synthesis inhibitor cycloheximide [8].

Chemical compound and disease context of Human papillomavirus 18


Biological context of Human papillomavirus 18


Anatomical context of Human papillomavirus 18

  • We found that FAK expression and activity were significantly elevated in HPV-18 E6/E7-immortalized human genital epithelial cells relative to their primary cell counterparts [9].
  • The human papillomavirus type 18 (HPV-18) E7 protein promotes S-phase reentry in postmitotic, differentiated keratinocytes in squamous epithelium to facilitate vegetative viral DNA amplification [12].
  • The glycolytic pathway inhibitor 2-deoxyglucose (2-DG) is capable of suppressing the transcription of the human pathogenic papillomavirus type 18 (HPV 18) in cervical carcinoma cells and derived non-tumorigenic somatic cell hybrids at the level of transcription initiation [18].
  • Low levels of AP1 in the fibroblasts correlate with the low activity of AP1-dependent promoters, like that of HPV-18, in these cells [19].
  • CD4(+) T cells from 16 healthy donors were tested ex vivo for reactivity to synthetic peptides corresponding to 3 sequences on the HPV-18 E6 transforming protein predicted by bioinformatics as promiscuous HLA-DR ligands, and to the recombinant E6 protein [20].

Gene context of Human papillomavirus 18


Analytical, diagnostic and therapeutic context of Human papillomavirus 18


  1. Chemoradiation of cervical cancer cells: targeting human papillomavirus E6 and p53 leads to either augmented or attenuated apoptosis depending on the platinum carrier ligand. Koivusalo, R., Krausz, E., Ruotsalainen, P., Helenius, H., Hietanen, S. Cancer Res. (2002) [Pubmed]
  2. HPV E6 proteins interact with specific PML isoforms and allow distinctions to be made between different POD structures. Guccione, E., Lethbridge, K.J., Killick, N., Leppard, K.N., Banks, L. Oncogene (2004) [Pubmed]
  3. Viability of wild type p53-containing and p53-deficient tumor cells following anticancer treatment: the use of human papillomavirus E6 to target p53. Labrecque, S., Matlashewski, G.J. Oncogene (1995) [Pubmed]
  4. Activation of human papillomavirus type 18 gene expression by herpes simplex virus type 1 viral transactivators and a phorbol ester. Gius, D., Laimins, L.A. J. Virol. (1989) [Pubmed]
  5. Transcription factor YY1 represses cell-free replication from human papillomavirus origins. Lee, K.Y., Broker, T.R., Chow, L.T. J. Virol. (1998) [Pubmed]
  6. The functional BPV-1 E2 trans-activating protein can act as a repressor by preventing formation of the initiation complex. Dostatni, N., Lambert, P.F., Sousa, R., Ham, J., Howley, P.M., Yaniv, M. Genes Dev. (1991) [Pubmed]
  7. Identification of a negative regulatory domain in the human papillomavirus type 18 promoter: interaction with the transcriptional repressor YY1. Bauknecht, T., Angel, P., Royer, H.D., zur Hausen, H. EMBO J. (1992) [Pubmed]
  8. Selective suppression of human papillomavirus transcription in non-tumorigenic cells by 5-azacytidine. Rösl, F., Dürst, M., zur Hausen, H. EMBO J. (1988) [Pubmed]
  9. Activation of the focal adhesion kinase signal transduction pathway in cervical carcinoma cell lines and human genital epithelial cells immortalized with human papillomavirus type 18. McCormack, S.J., Brazinski, S.E., Moore, J.L., Werness, B.A., Goldstein, D.J. Oncogene (1997) [Pubmed]
  10. Cell-type-specific activity of the human papillomavirus type 18 upstream regulatory region in transgenic mice and its modulation by tetradecanoyl phorbol acetate and glucocorticoids. Cid, A., Auewarakul, P., Garcia-Carranca, A., Ovseiovich, R., Gaissert, H., Gissmann, L. J. Virol. (1993) [Pubmed]
  11. Human papillomavirus type 18 E7 protein requires intact Cys-X-X-Cys motifs for zinc binding, dimerization, and transformation but not for Rb binding. McIntyre, M.C., Frattini, M.G., Grossman, S.R., Laimins, L.A. J. Virol. (1993) [Pubmed]
  12. Alternative fates of keratinocytes transduced by human papillomavirus type 18 E7 during squamous differentiation. Chien, W.M., Noya, F., Benedict-Hamilton, H.M., Broker, T.R., Chow, L.T. J. Virol. (2002) [Pubmed]
  13. Expression of cytochrome P450 and microsomal epoxide hydrolase in cervical and oral epithelial cells immortalized by human papillomavirus type 16 E6/E7 genes. Farin, F.M., Bigler, L.G., Oda, D., McDougall, J.K., Omiecinski, C.J. Carcinogenesis (1995) [Pubmed]
  14. E1 protein of human papillomavirus type 1a is sufficient for initiation of viral DNA replication. Gopalakrishnan, V., Khan, S.A. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  15. Amplification of the integrated viral transforming genes of human papillomavirus 18 and its 5'-flanking cellular sequence located near the myc protooncogene in HeLa cells. Lazo, P.A., DiPaolo, J.A., Popescu, N.C. Cancer Res. (1989) [Pubmed]
  16. cAMP response element-binding protein-binding protein binds to human papillomavirus E2 protein and activates E2-dependent transcription. Lee, D., Lee, B., Kim, J., Kim, D.W., Choe, J. J. Biol. Chem. (2000) [Pubmed]
  17. The structural basis of DNA target discrimination by papillomavirus E2 proteins. Kim, S.S., Tam, J.K., Wang, A.F., Hegde, R.S. J. Biol. Chem. (2000) [Pubmed]
  18. Selective down-regulation of human papillomavirus transcription by 2-deoxyglucose. Maehama, T., Patzelt, A., Lengert, M., Hutter, K.J., Kanazawa, K., Hausen, H., Rösl, F. Int. J. Cancer (1998) [Pubmed]
  19. Different stability of AP1 proteins in human keratinocyte and fibroblast cells: possible role in the cell-type specific expression of human papillomavirus type 18 genes. Offord, E.A., Chappuis, P.O., Beard, P. Carcinogenesis (1993) [Pubmed]
  20. CD4+ T cell immunity against the human papillomavirus-18 E6 transforming protein in healthy donors: identification of promiscuous naturally processed epitopes. Facchinetti, V., Seresini, S., Longhi, R., Garavaglia, C., Casorati, G., Protti, M.P. Eur. J. Immunol. (2005) [Pubmed]
  21. HeLa cells are phenotypically limiting in cyclin E/CDK2 for efficient human papillomavirus DNA replication. Lin, B.Y., Ma, T., Liu, J.S., Kuo, S.R., Jin, G., Broker, T.R., Harper, J.W., Chow, L.T. J. Biol. Chem. (2000) [Pubmed]
  22. Interferon regulatory factor-1 (IRF-1) is a mediator for interferon-gamma induced attenuation of telomerase activity and human telomerase reverse transcriptase (hTERT) expression. Lee, S.H., Kim, J.W., Lee, H.W., Cho, Y.S., Oh, S.H., Kim, Y.J., Jung, C.H., Zhang, W., Lee, J.H. Oncogene (2003) [Pubmed]
  23. The human papilloma virus (HPV)-18 E6 oncoprotein physically associates with Tyk2 and impairs Jak-STAT activation by interferon-alpha. Li, S., Labrecque, S., Gauzzi, M.C., Cuddihy, A.R., Wong, A.H., Pellegrini, S., Matlashewski, G.J., Koromilas, A.E. Oncogene (1999) [Pubmed]
  24. Differential transcriptional regulation of the monocyte-chemoattractant protein-1 (MCP-1) gene in tumorigenic and non-tumorigenic HPV 18 positive cells: the role of the chromatin structure and AP-1 composition. Finzer, P., Soto, U., Delius, H., Patzelt, A., Coy, J.F., Poustka, A., zur Hausen, H., Rösl, F. Oncogene (2000) [Pubmed]
  25. Identification of B-epitopes in the human papillomavirus 18 E7 open reading frame protein. Selvey, L.A., Tindle, R.W., Geysen, H.M., Haller, C.J., Smith, J.A., Frazer, I.H. J. Immunol. (1990) [Pubmed]
  26. Herpes simplex virus and risk of cervical cancer: a longitudinal, nested case-control study in the nordic countries. Lehtinen, M., Koskela, P., Jellum, E., Bloigu, A., Anttila, T., Hallmans, G., Luukkaala, T., Thoresen, S., Youngman, L., Dillner, J., Hakama, M. Am. J. Epidemiol. (2002) [Pubmed]
  27. Human immunodeficiency virus infection in vitro activates naturally integrated human papillomavirus type 18 and induces synthesis of the L1 capsid protein. Dolei, A., Curreli, S., Marongiu, P., Pierangeli, A., Gomes, E., Bucci, M., Serra, C., Degener, A.M. J. Gen. Virol. (1999) [Pubmed]
  28. HPV oligonucleotide microarray-based detection of HPV genotypes in cervical neoplastic lesions. Kim, C.J., Jeong, J.K., Park, M., Park, T.S., Park, T.C., Namkoong, S.E., Park, J.S. Gynecol. Oncol. (2003) [Pubmed]
  29. Squamous cell carcinoma of the cervix: HPV 16 and DNA ploidy as predictors of survival. Jarrell, M.A., Heintz, N., Howard, P., Collins, C., Badger, G., Belinson, J., Nason, F. Gynecol. Oncol. (1992) [Pubmed]
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