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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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Bibliographic Details
Main Authors: Carmen Aguilar Lemarroy, Adriana del (Author) , Zur Hausen, Harald (Author) , Krammer, Peter H. (Author) , Rösl, Frank (Author)
Format: Article (Journal)
Language:English
Published: 13 August 2001
In: International journal of cancer
Year: 2001, Volume: 93, Issue: 6, Pages: 823-831
ISSN:1097-0215
DOI:https://doi.org/10.1002/ijc.1405
Online Access: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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Author Notes:Adriana Aguilar‐Lemarroy, Sabine Kirchhoff, Noel Whitaker, Patricio Gariglio, Harald zur Hausen, Peter H. Krammer and Frank Rösl
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Summary: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.
Item Description:Gesehen am 27.04.2021
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Physical Description:Online Resource
ISSN:1097-0215
DOI:https://doi.org/10.1002/ijc.1405

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