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dc.contributor.authorYu, Lunyin
dc.contributor.authorGarg, Hari G.
dc.contributor.authorLi, Boyangzi
dc.contributor.authorLinhardt, Robert J.
dc.contributor.authorHales, Charles A.
dc.date2010
dc.date.accessioned2022-06-27T16:10:54Z
dc.date.available2022-06-27T16:10:54Z
dc.date.issued2010-03-01
dc.identifier.citationAntitumor effect of butanoylated heparin with low anticoagulant activity on lung cancer growth in mice and rats, L. Yu, H. G. Garg, B. Li, R. J. Linhardt, C. A. Hales, Current Cancer Drug Targets, 10, 229-241, 2010.
dc.identifier.issn15680096
dc.identifier.urihttps://doi.org/10.2174/156800910791054176
dc.identifier.urihttps://hdl.handle.net/20.500.13015/5741
dc.descriptionCurrent Cancer Drug Targets, 10, 229-241
dc.descriptionNote : if this item contains full text it may be a preprint, author manuscript, or a Gold OA copy that permits redistribution with a license such as CC BY. The final version is available through the publisher’s platform.
dc.description.abstractWhole unfractionated heparin can modestly decrease tumor growth, but the dose of heparin is limited by its anticoagulant properties. To overcome this limitation, we modified the chemical structure of heparin and have prepared a heparin derivative by O-acylating low molecular weight heparin with butyric anhydride, producing a more potent antiproliferative compound, which is only weakly anticoagulant so that the dose may be escalated without threat of hemorrhage. In this study, we investigated the effect of this chemically modified heparin, butanoylated heparin, on the growth of lung cancer in vitro and in vivo. We found that butanoylated heparin a) significantly inhibited lung cancer cell proliferation in vitro and lung cancer growth in mice and rats; b) had very low anticoagulant effect; c) had no significant toxicity on heart, liver, kidney and lung; d) significantly although modestly induced apoptosis and decreased expression of the cell proliferation pathway consisting of mutant p53, phospho-Rb and E2F1 expression in the tumor tissues. We also found that butanoylated heparin significantly inhibited CXCL12 and CXCR4 expression, suggesting that CXCL12/CXCR4 axis may be involved in regulation of tumor growth inhibition by heparin. We concluded that chemically modified butanoylated heparin has potent antiproliferative activity against lung cancer and may represent a new chemical therapeutic agent for cancer patients.
dc.description.sponsorshipNational Heart, Lung, and Blood Institute
dc.description.urihttps://login.libproxy.rpi.edu/login?url=https://doi.org/10.2174/156800910791054176
dc.languageen_US
dc.language.isoENG
dc.relation.ispartofThe Linhardt Research Labs Online Collection
dc.relation.ispartofRensselaer Polytechnic Institute, Troy, NY
dc.relation.ispartofCurrent Cancer Drug Targets
dc.relation.urihttps://harc.rpi.edu/
dc.subjectBiology
dc.subjectChemistry and chemical biology
dc.subjectChemical and biological engineering
dc.subjectBiomedical engineering
dc.titleAntitumor effect of butanoylated heparin with low anticoagulant activity on lung cancer growth in mice and rats
dc.typeArticle
dcterms.accessRightshttps://login.libproxy.rpi.edu/login?url=https://doi.org/10.2174/156800910791054176
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dcterms.isVersionOfhttps://doi.org/10.2174/156800910791054176
dc.rights.holderIn Copyright : this Item is protected by copyright and/or related rights. You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s). https://rightsstatements.org/page/InC/1.0/
dc.creator.identifierhttps://orcid.org/0000-0003-2219-5833
dc.relation.departmentThe Linhardt Research Labs.
dc.relation.departmentThe Shirley Ann Jackson, Ph.D. Center for Biotechnology and Interdisciplinary Studies (CBIS)
rpi.description.pages229-241
rpi.description.volume10


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