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

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dc.contributor.authorRyan, Aideen E.
dc.contributor.authorLane, Sinead
dc.contributor.authorShanahan, Fergus
dc.contributor.authorO'Connell, Joe
dc.contributor.authorHouston, Aileen M.
dc.contributor.funderScience Foundation Irelanden
dc.contributor.funderEnterprise Irelanden
dc.contributor.funderWellcome Trusten
dc.contributor.funderHealth Research Boarden
dc.contributor.funderHigher Education Authorityen
dc.date.accessioned2013-01-29T14:22:55Z
dc.date.available2013-01-29T14:22:55Z
dc.date.copyright2006
dc.date.issued2006-02-02
dc.description.abstractBackground: 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.sponsorshipScience Foundation Ireland (SFI-CSET)en
dc.description.statusPeer revieweden
dc.description.versionPublished Versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.citationRyan, 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: 10.1186/1477-3163-5-5en
dc.identifier.doi10.1186/1477-3163-5-5
dc.identifier.endpage5-7en
dc.identifier.issn0974-6773
dc.identifier.journaltitleJournal of Carcinogenesisen
dc.identifier.startpage5-1en
dc.identifier.urihttps://hdl.handle.net/10468/941
dc.identifier.volume5en
dc.language.isoenen
dc.publisherMedknow Publicationsen
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.urihttp://creativecommons.org/licenses/by/2.0/en
dc.subjectFas Ligand (FasL/CD95L) expressionen
dc.subjectCarcinogenesisen
dc.subjectApoptosisen
dc.subjectTumoren
dc.subjectTumouren
dc.subjectWestern blottingen
dc.subjectIntron spanning primersen
dc.subjectImmunofluorescenceen
dc.titleFas ligand expression in human and mouse cancer cell lines; a caveat on over-reliance on mRNA dataen
dc.typeArticle (peer-reviewed)en
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