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Article: Lipocalin 2 performs contrasting, location-dependent roles in APCmin tumor initiation and progression

TitleLipocalin 2 performs contrasting, location-dependent roles in APCmin tumor initiation and progression
Authors
Keywordsiron
intestinal cancer
24p3
NGAL
Issue Date2013
Citation
Oncogene, 2013, v. 32, n. 10, p. 1233-1239 How to Cite?
AbstractEvidence that lipocalin 2 (LCN2) is oncogenic has grown in recent years and comes from both animal models and expression analysis from a variety of human cancers. In the intestine, LCN2 is overexpressed in colitis patients and its overexpression is a negative prognostic indicator in colorectal cancer. Functionally, LCN2 has a number of different activities that may contribute to its oncogenic potential, including increasing matrix metalloproteinase activity, control of iron availability and stimulating inflammation. In this report, we examined APCmin intestinal tumorigenesis in an LCN2-deficient background. We found that the loss of LCN2 increased tumor multiplicity specifically in the duodenum, suggesting a potential tumor-suppressive activity. Concurrently, however, LCN2 increased the average small intestinal tumor size particularly in the distal small intestine. We found that this increase was correlated to tumor iron(II) content, suggesting that an iron-scavenging role is important for LCN2 oncogenic activity in the intestine. © 2013 Macmillan Publishers Limited.
Persistent Identifierhttp://hdl.handle.net/10722/292231
ISSN
2023 Impact Factor: 6.9
2023 SCImago Journal Rankings: 2.334
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorReilly, P. T.-
dc.contributor.authorTeo, W. L.-
dc.contributor.authorLow, M. J.-
dc.contributor.authorAmoyo-Brion, A. A.-
dc.contributor.authorDominguez-Brauer, C.-
dc.contributor.authorElia, A. J.-
dc.contributor.authorBerger, T.-
dc.contributor.authorGreicius, G.-
dc.contributor.authorPettersson, S.-
dc.contributor.authorMak, T. W.-
dc.date.accessioned2020-11-17T14:56:02Z-
dc.date.available2020-11-17T14:56:02Z-
dc.date.issued2013-
dc.identifier.citationOncogene, 2013, v. 32, n. 10, p. 1233-1239-
dc.identifier.issn0950-9232-
dc.identifier.urihttp://hdl.handle.net/10722/292231-
dc.description.abstractEvidence that lipocalin 2 (LCN2) is oncogenic has grown in recent years and comes from both animal models and expression analysis from a variety of human cancers. In the intestine, LCN2 is overexpressed in colitis patients and its overexpression is a negative prognostic indicator in colorectal cancer. Functionally, LCN2 has a number of different activities that may contribute to its oncogenic potential, including increasing matrix metalloproteinase activity, control of iron availability and stimulating inflammation. In this report, we examined APCmin intestinal tumorigenesis in an LCN2-deficient background. We found that the loss of LCN2 increased tumor multiplicity specifically in the duodenum, suggesting a potential tumor-suppressive activity. Concurrently, however, LCN2 increased the average small intestinal tumor size particularly in the distal small intestine. We found that this increase was correlated to tumor iron(II) content, suggesting that an iron-scavenging role is important for LCN2 oncogenic activity in the intestine. © 2013 Macmillan Publishers Limited.-
dc.languageeng-
dc.relation.ispartofOncogene-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectiron-
dc.subjectintestinal cancer-
dc.subject24p3-
dc.subjectNGAL-
dc.titleLipocalin 2 performs contrasting, location-dependent roles in APCmin tumor initiation and progression-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/onc.2012.159-
dc.identifier.pmid22614012-
dc.identifier.pmcidPMC3594828-
dc.identifier.scopuseid_2-s2.0-84874766439-
dc.identifier.volume32-
dc.identifier.issue10-
dc.identifier.spage1233-
dc.identifier.epage1239-
dc.identifier.eissn1476-5594-
dc.identifier.isiWOS:000316454500004-
dc.identifier.issnl0950-9232-

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