Differential sensitivity of human papillomavirus type 16+ and type 18+ cervical carcinoma cells to CD95-mediated apoptosis
When cervical carcinoma cells were monitored for apoptotic signals, HPV18+ lines were found to be highly sensitive to agonistic CD95 antibodies or recombinant CD95 ligands after co-exposure with CHX (CD95S). In contrast, HPV16+ cervical carcinoma cells and HPV16-immortalized non-malignant human kera...
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| Hauptverfasser: | , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
13 August 2001
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| In: |
International journal of cancer
Year: 2001, Jahrgang: 93, Heft: 6, Pages: 823-831 |
| ISSN: | 1097-0215 |
| DOI: | https://doi.org/10.1002/ijc.1405 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/https://doi.org/10.1002/ijc.1405 Verlag, lizenzpflichtig, Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1002/ijc.1405 
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| Verfasserangaben: | Adriana Aguilar‐Lemarroy, Sabine Kirchhoff, Noel Whitaker, Patricio Gariglio, Harald zur Hausen, Peter H. Krammer and Frank Rösl |
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| 245 | 1 | 0 | |a Differential sensitivity of human papillomavirus type 16+ and type 18+ cervical carcinoma cells to CD95-mediated apoptosis |c Adriana Aguilar‐Lemarroy, Sabine Kirchhoff, Noel Whitaker, Patricio Gariglio, Harald zur Hausen, Peter H. Krammer and Frank Rösl |
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| 520 | |a When cervical carcinoma cells were monitored for apoptotic signals, HPV18+ lines were found to be highly sensitive to agonistic CD95 antibodies or recombinant CD95 ligands after co-exposure with CHX (CD95S). In contrast, HPV16+ cervical carcinoma cells and HPV16-immortalized non-malignant human keratinocytes were CD95-resistant (CD95R) under equivalent conditions. Somatic cell hybridization between CD95S and CD95R cervical carcinoma cell lines revealed that CD95 sensitivity was a dominant trait, which could be correlated with abundant c-Myc and low Bcl-XL expression. Although CD95R cervical carcinoma cells expressed even higher levels of p53 and CD95 receptor at the surface, resistance could be attributed to the inability to form a functional DISC, necessary for successful transmission of the apoptogenic response. These data indicate that resistance to apoptotic stimuli represents an important immunological escape mechanism during virus-induced carcinogenesis. | ||
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