Document Detail


Thrombospondin-1 associated with tumor microenvironment contributes to low-dose cyclophosphamide-mediated endothelial cell apoptosis and tumor growth suppression.
MedLine Citation:
PMID:  14996710     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Low-dose cyclophosphamide (LDC) induces selective apoptosis of endothelial cells within the vascular bed of tumors. Here, we investigated a hypothesis that the effect of LDC is mediated by the pro-apoptotic action of endogenous inhibitors of angiogenesis. Tumors treated with LDC demonstrate similar expression of matrix metalloproteinases and also basement membrane-derived angiogenesis inhibitors when compared with wild-type tumors, whereas the expression of thrombospondin-1 (TSP-1) is significantly elevated in LDC-treated tumors. We used mice with an absence of type XVIII collagen (endostatin) or type IV collagen alpha3 chain (tumstatin) or TSP-1 to assess the contribution of these endogenous inhibitors of angiogenesis on LDC-mediated tumor suppression. Lack of TSP-1 in the host in addition to tumor cells leads to diminished capacity of LDC to suppress tumor growth, whereas the absence of endostatin and tumstatin did not alter the effect of LDC. LDC treatment predominantly induces selective expression of TSP-1 in tumor cells and peri-vascular cells and facilitates apoptosis of proliferating endothelial cells, with minimal direct effect on tumor cells and peri-vascular cells. These studies indicate that TSP-1 contributes to tumor growth suppression induced by LDC and suggest that tumors that express high basal level of TSP-1 may be more susceptible to tumor suppression by such a regimen. This study also makes a strong case for TSP-1 expression levels as a potential predictive marker for the successful use of LDC in cancer patients.
Authors:
Yuki Hamano; Hikaru Sugimoto; Mary A Soubasakos; Mark Kieran; Bjorn R Olsen; Jack Lawler; Akulapalli Sudhakar; Raghu Kalluri
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Cancer research     Volume:  64     ISSN:  0008-5472     ISO Abbreviation:  Cancer Res.     Publication Date:  2004 Mar 
Date Detail:
Created Date:  2004-03-03     Completed Date:  2004-03-31     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1570-4     Citation Subset:  IM    
Affiliation:
Center for Matrix Biology, Department of Medicine and the Cancer Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
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MeSH Terms
Descriptor/Qualifier:
Angiogenesis Inhibitors / pharmacology*
Animals
Apoptosis / drug effects*
Autoantigens / physiology
Cell Division / drug effects
Cell Survival / drug effects
Collagen Type IV / physiology
Cyclophosphamide / pharmacology*,  therapeutic use
Endostatins / physiology
Endothelial Cells / drug effects*,  pathology
Matrix Metalloproteinases / analysis
Mice
Mice, Inbred C57BL
NIH 3T3 Cells
Neoplasms, Experimental / drug therapy*
Thrombospondin 1 / analysis,  physiology*
Grant Support
ID/Acronym/Agency:
DK 55001/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Angiogenesis Inhibitors; 0/Autoantigens; 0/Collagen Type IV; 0/Endostatins; 0/Thrombospondin 1; 0/type IV collagen alpha3 chain; 50-18-0/Cyclophosphamide; EC 3.4.24.-/Matrix Metalloproteinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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