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dc.contributor.authorHeidemann, Franziska
dc.contributor.authorSchildt, Anna
dc.contributor.authorSchmid, Katharina
dc.contributor.authorBruns, Oliver Thomas
dc.contributor.authorRiecken, Kristoffer
dc.contributor.authorJung, Caroline
dc.contributor.authorIttrich, Harald
dc.contributor.authorWicklein, Daniel
dc.contributor.authorReimer, Rudolph
dc.contributor.authorFehse, Boris
dc.contributor.authorHeeren, Joerg
dc.contributor.authorLüers, Georg
dc.contributor.authorSchumacher, Udo
dc.contributor.authorHeine, Markus
dc.date.accessioned2014-06-23T14:38:15Z
dc.date.available2014-06-23T14:38:15Z
dc.date.issued2014-04
dc.identifier.issn1932-6203
dc.identifier.urihttp://hdl.handle.net/1721.1/88056
dc.description.abstractMetastasis formation is the major reason for the extremely poor prognosis in small cell lung cancer (SCLC) patients. The molecular interaction partners regulating metastasis formation in SCLC are largely unidentified, however, from other tumor entities it is known that tumor cells use the adhesion molecules of the leukocyte adhesion cascade to attach to the endothelium at the site of the future metastasis. Using the human OH-1 SCLC line as a model, we found that these cells expressed E- and P-selectin binding sites, which could be in part attributed to the selectin binding carbohydrate motif sialyl Lewis A. In addition, protein backbones known to carry these glycotopes in other cell lines including PSGL-1, CD44 and CEA could be detected in in vitro and in vivo grown OH1 SCLC cells. By intravital microscopy of murine mesenterial vasculature we could capture SCLC cells while rolling along vessel walls demonstrating that SCLC cells mimic leukocyte rolling behavior in terms of selectin and selectin ligand interaction in vivo indicating that this mechanism might indeed be important for SCLC cells to seed distant metastases. Accordingly, formation of spontaneous distant metastases was reduced by 50% when OH-1 cells were xenografted into E-/P-selectin-deficient mice compared with wild type mice (p = 0.0181). However, as metastasis formation was not completely abrogated in selectin deficient mice, we concluded that this adhesion cascade is redundant and that other molecules of this cascade mediate metastasis formation as well. Using several of these adhesion molecules as interaction partners presumably make SCLC cells so highly metastatic.en_US
dc.description.sponsorshipBundesministerium für Wissenschaft und Forschung (TOMCAT, grant number 01EZ0824; http://www.bmbf.de/)en_US
dc.description.sponsorshipLandesexzellenzinitiative Hamburg (Nanotechnology in Medicine – NAME)en_US
dc.language.isoen_US
dc.publisherPublic Library of Scienceen_US
dc.relation.isversionofhttp://dx.doi.org/10.1371/journal.pone.0092327en_US
dc.rightsCreative Commons Attributionen_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_US
dc.sourcePublic Library of Scienceen_US
dc.titleSelectins Mediate Small Cell Lung Cancer Systemic Metastasisen_US
dc.typeArticleen_US
dc.identifier.citationHeidemann, Franziska, Anna Schildt, Katharina Schmid, Oliver T. Bruns, Kristoffer Riecken, Caroline Jung, Harald Ittrich, et al. “Selectins Mediate Small Cell Lung Cancer Systemic Metastasis.” Edited by Andreas-Claudius Hoffmann. PLoS ONE 9, no. 4 (April 3, 2014): e92327.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Chemistryen_US
dc.contributor.mitauthorBruns, Oliver Thomasen_US
dc.relation.journalPLoS ONEen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsHeidemann, Franziska; Schildt, Anna; Schmid, Katharina; Bruns, Oliver T.; Riecken, Kristoffer; Jung, Caroline; Ittrich, Harald; Wicklein, Daniel; Reimer, Rudolph; Fehse, Boris; Heeren, Joerg; Lüers, Georg; Schumacher, Udo; Heine, Markusen_US
mit.licensePUBLISHER_CCen_US


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