Fas ligand expression in human and mouse cancer cell lines; a caveat on over-reliance on mRNA data

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dc.contributor.author Ryan, Aideen E.
dc.contributor.author Lane, Sinead
dc.contributor.author Shanahan, Fergus
dc.contributor.author O'Connell, Joe
dc.contributor.author Houston, Aileen M.
dc.date.accessioned 2013-01-29T14:22:55Z
dc.date.available 2013-01-29T14:22:55Z
dc.date.copyright 2006
dc.date.issued 2006-02-02
dc.identifier.citation Ryan, A., Lane, S., Shanahan, F., O'Connell, J. and Houston, A. (2006) 'Fas ligand expression in human and mouse cancer cell lines; a caveat on over-reliance on mRNA data', Journal of Carcinogenesis, 5, 5 (7 pp). doi: 10.1186/1477-3163-5-5 en
dc.identifier.volume 5 en
dc.identifier.startpage 5-1 en
dc.identifier.endpage 5-7 en
dc.identifier.issn 0974-6773
dc.identifier.uri http://hdl.handle.net/10468/941
dc.identifier.doi 10.1186/1477-3163-5-5
dc.description.abstract Background: During carcinogenesis, tumors develop multiple mechanisms for evading the immune response, including upregulation of Fas ligand (FasL/CD95L) expression. Expression of FasL may help to maintain tumor cells in a state of immune privilege by inducing apoptosis of antitumor immune effector cells. Recently this idea has been challenged by studies reporting that tumor cells of varying origin do not express FasL. In the present study, we aimed to comprehensively characterize FasL expression in tumors of both murine and human origin over a 72 hour time period. Methods: RNA and protein was extracted from six human (SW620, HT29, SW480, KM12SM,HCT116, Jurkat) and three mouse (CMT93, CT26, B16F10) cancer cell lines at regular time intervals over a 72 hour time period. FasL expression was detected at the mRNA level by RT-PCR, using intron spanning primers, and at the protein level by Western Blotting and immunofluorescence, using a polyclonal FasL- specific antibody. Results: Expression of FasL mRNA and protein was observed in all cell lines analysed. However, expression of FasL mRNA varied dramatically over time, with cells negative for FasL mRNA at many time points. In contrast, 8 of the 9 cell lines constitutively expressed FasL protein. Thus, cells can abundantly express FasL protein at times when FasL mRNA is absent. Conclusion: These findings demonstrate the importance of complete analysis of FasL expression by tumor cells in order to fully characterize its biological function and may help to resolve the discrepancies present in the literature regarding FasL expression and tumor immune privilege. en
dc.description.sponsorship Science Foundation Ireland (SFI-CSET) en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Medknow Publications en
dc.rights © 2006 Ryan et al; This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. en
dc.rights.uri http://creativecommons.org/licenses/by/2.0/ en
dc.subject Fas Ligand (FasL/CD95L) expression en
dc.subject Carcinogenesis en
dc.subject Apoptosis en
dc.subject Tumor en
dc.subject Tumour en
dc.subject Western blotting en
dc.subject Intron spanning primers en
dc.subject Immunofluorescence en
dc.title Fas ligand expression in human and mouse cancer cell lines; a caveat on over-reliance on mRNA data en
dc.type Article (peer-reviewed) en
dc.internal.authorurl http://research.ucc.ie/profiles/C012/fshanahan en
dc.internal.authorcontactother Alimentary Pharmabiotic Centre, University College Cork, College Road, Cork, Ireland. Email: f.shanahan@ucc.ie en
dc.internal.authorcontactother Aileen Houston, Medicine Department , University College Cork, Cork, Ireland. +353-21-490-3000 Email: a.houston@ucc.ie en
dc.internal.availability Full text available en
dc.description.version Published Version en
dc.internal.rssid 122827868
dc.internal.rssid 356423
dc.contributor.funder Science Foundation Ireland en
dc.contributor.funder Enterprise Ireland en
dc.contributor.funder Wellcome Trust en
dc.contributor.funder Health Research Board en
dc.contributor.funder Higher Education Authority en
dc.description.status Peer reviewed en
dc.identifier.journaltitle Journal of Carcinogenesis en
dc.internal.copyrightchecked Journal of Carcinogenesis, accessed via BioMed Central, is available as Open Access. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Creative Commons: You are free: to Share — to copy, distribute and transmit the work to Remix — to adapt the work to make commercial use of the work Under the following conditions: Attribution — You must attribute the work in the manner specified by the author or licensor (but not in any way that suggests that they endorse you or your use of the work). With the understanding that: Waiver— Any of the above conditions can be waived if you get permission from the copyright holder. Public Domain— Where the work or any of its elements is in the public domain under applicable law, that status is in no way affected by the license. Other Rights— In no way are any of the following rights affected by the license: • Your fair dealing or fair use rights, or other applicable copyright exceptions and limitations; • The author's moral rights; • Rights other persons may have either in the work itself or in how the work is used, such as publicity or privacy rights. Notice— For any reuse or distribution, you must make clear to others the license terms of this work. The best way to do this is with a link to this web page. en
dc.internal.IRISemailaddress f.shanahan@ucc.ie en
dc.internal.IRISemailaddress a.houston@ucc.ie en


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© 2006 Ryan et al; This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Except where otherwise noted, this item's license is described as © 2006 Ryan et al; This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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