Abstract:
:Inhibiting angiogenesis has become a major therapeutic strategy for cancer treatment. To identify common intracellular mediators, we previously analyzed gene expression profiles of endothelial cells after treatment with angiogenesis inhibitors. Filamin A interacting protein 1-like (FILIP1L; previously known as down-regulated in ovarian cancer 1) was identified as one of the genes up-regulated in endothelial cells in response to these inhibitors. However, the expression and function of FILIP1L protein is uncharacterized. Here, we provide the first description of the expression and specific subcellular localization of FILIP1L protein in human tissue. Overexpression of FILIP1L resulted in inhibition of cell proliferation and migration and increased apoptosis. In addition, overexpression of FILIP1L truncation mutants showed differential antiproliferative activity. A COOH terminal truncation mutant (FILIP1LDeltaC103) was more potent than wild-type FILIP1L in mediating this activity. Targeted expression of FILIP1LDeltaC103 in tumor vasculature inhibited tumor growth in vivo. Overall, these findings suggest that the novel protein FILIP1L may be an important mediator of the effects of angiogenesis inhibitors and that FILIP1L has the potential to be an antivascular reagent for cancer therapy.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Kwon M,Hanna E,Lorang D,He M,Quick JS,Adem A,Stevenson C,Chung JY,Hewitt SM,Zudaire E,Esposito D,Cuttitta F,Libutti SKdoi
10.1158/0008-5472.CAN-08-1087subject
Has Abstractpub_date
2008-09-15 00:00:00pages
7332-41issue
18eissn
0008-5472issn
1538-7445pii
68/18/7332journal_volume
68pub_type
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